SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation

Cancer is currently one of the major causes of death in patients with type 2 diabetes mellitus. We previously reported the beneficial effects of the glucagon-like peptide-1 receptor agonist exendin-4 against prostate and breast cancer. In the present study, we examined the anti-cancer effect of the...

Full description

Saved in:

Bibliographic Details
Published in	ENDOCRINE JOURNAL Vol. 67; no. 1; pp. 99 - 106
Main Authors	Komatsu, Shiho, Nomiyama, Takashi, Numata, Tomohiro, Kawanami, Takako, Hamaguchi, Yuriko, Iwaya, Chikayo, Horikawa, Tsuyoshi, Fujimura-Tanaka, Yuki, Hamanoue, Nobuya, Motonaga, Ryoko, Tanabe, Makito, Inoue, Ryuji, Yanase, Toshihiko, Kawanami, Daiji
Format	Journal Article
Language	English
Published	Japan The Japan Endocrine Society 01.01.2020 Japan Science and Technology Agency
Subjects	Breast cancer Cell growth Cell proliferation Diabetes mellitus (non-insulin dependent) Glucagon Glucagon-like peptide 1 Glucose Hyperpolarization Immunohistochemistry Membrane potential Mitochondria Na+/glucose cotransporter Polymerase chain reaction Prostate cancer SGLT2 inhibitor siRNA Mitochondria Breast cancer Membrane potential SGLT2 inhibitor
Online Access	Get full text

Cover

Loading…

Abstract	Cancer is currently one of the major causes of death in patients with type 2 diabetes mellitus. We previously reported the beneficial effects of the glucagon-like peptide-1 receptor agonist exendin-4 against prostate and breast cancer. In the present study, we examined the anti-cancer effect of the sodium-glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin using a breast cancer model. In human breast cancer MCF-7 cells, SGLT2 expression was detected using both RT-PCR and immunohistochemistry. Ipragliflozin at 1–50 μM significantly and dose-dependently suppressed the growth of MCF-7 cells. BrdU assay also revealed that ipragliflozin attenuated the proliferation of MCF-7 cells in a dose-dependent manner. Because the effect of ipragliflozin against breast cancer cells was completely canceled by knocking down SGLT2, ipragliflozin could act via inhibiting SGLT2. We next measured membrane potential and whole-cell current using the patch clamp technique. When we treated MCF-7 cells with ipragliflozin or glucose-free medium, membrane hyperpolarization was observed. In addition, glucose-free medium and knockdown of SGLT2 by siRNA suppressed the glucose-induced whole-cell current of MCF-7 cells, suggesting that ipragliflozin inhibits sodium and glucose cotransport through SGLT2. Furthermore, JC-1 green fluorescence was significantly increased by ipragliflozin, suggesting the change of mitochondrial membrane potential. These findings suggest that the SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation via membrane hyperpolarization and mitochondrial membrane instability.
AbstractList	Cancer is currently one of the major causes of death in patients with type 2 diabetes mellitus. We previously reported the beneficial effects of the glucagon-like peptide-1 receptor agonist exendin-4 against prostate and breast cancer. In the present study, we examined the anti-cancer effect of the sodium-glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin using a breast cancer model. In human breast cancer MCF-7 cells, SGLT2 expression was detected using both RT-PCR and immunohistochemistry. Ipragliflozin at 1–50 μM significantly and dose-dependently suppressed the growth of MCF-7 cells. BrdU assay also revealed that ipragliflozin attenuated the proliferation of MCF-7 cells in a dose-dependent manner. Because the effect of ipragliflozin against breast cancer cells was completely canceled by knocking down SGLT2, ipragliflozin could act via inhibiting SGLT2. We next measured membrane potential and whole-cell current using the patch clamp technique. When we treated MCF-7 cells with ipragliflozin or glucose-free medium, membrane hyperpolarization was observed. In addition, glucose-free medium and knockdown of SGLT2 by siRNA suppressed the glucose-induced whole-cell current of MCF-7 cells, suggesting that ipragliflozin inhibits sodium and glucose cotransport through SGLT2. Furthermore, JC-1 green fluorescence was significantly increased by ipragliflozin, suggesting the change of mitochondrial membrane potential. These findings suggest that the SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation via membrane hyperpolarization and mitochondrial membrane instability. [Abstract.] Cancer is currently one of the major causes of death in patients with type 2 diabetes mellitus. We previously reported the beneficial effects of the glucagon-like peptide-1 receptor agonist exendin-4 against prostate and breast cancer. In the present study, we examined the anti-cancer effect of the sodium-glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin using a breast cancer model. In human breast cancer MCF-7 cells, SGLT2 expression was detected using both RT-PCR and immunohistochemistry. Ipragliflozin at 1-50 μM significantly and dose-dependently suppressed the growth of MCF-7 cells. BrdU assay also revealed that ipragliflozin attenuated the proliferation of MCF-7 cells in a dose-dependent manner. Because the effect of ipragliflozin against breast cancer cells was completely canceled by knocking down SGLT2, ipragliflozin could act via inhibiting SGLT2. We next measured membrane potential and whole-cell current using the patch clamp technique. When we treated MCF-7 cells with ipragliflozin or glucose-free medium, membrane hyperpolarization was observed. In addition, glucose-free medium and knockdown of SGLT2 by siRNA suppressed the glucose-induced whole-cell current of MCF-7 cells, suggesting that ipragliflozin inhibits sodium and glucose cotransport through SGLT2. Furthermore, JC-1 green fluorescence was significantly increased by ipragliflozin, suggesting the change of mitochondrial membrane potential. These findings suggest that the SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation via membrane hyperpolarization and mitochondrial membrane instability. Cancer is currently one of the major causes of death in patients with type 2 diabetes mellitus. We previously reported the beneficial effects of the glucagon-like peptide-1 receptor agonist exendin-4 against prostate and breast cancer. In the present study, we examined the anti-cancer effect of the sodium-glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin using a breast cancer model. In human breast cancer MCF-7 cells, SGLT2 expression was detected using both RT-PCR and immunohistochemistry. Ipragliflozin at 1-50 μM significantly and dose-dependently suppressed the growth of MCF-7 cells. BrdU assay also revealed that ipragliflozin attenuated the proliferation of MCF-7 cells in a dose-dependent manner. Because the effect of ipragliflozin against breast cancer cells was completely canceled by knocking down SGLT2, ipragliflozin could act via inhibiting SGLT2. We next measured membrane potential and whole-cell current using the patch clamp technique. When we treated MCF-7 cells with ipragliflozin or glucose-free medium, membrane hyperpolarization was observed. In addition, glucose-free medium and knockdown of SGLT2 by siRNA suppressed the glucose-induced whole-cell current of MCF-7 cells, suggesting that ipragliflozin inhibits sodium and glucose cotransport through SGLT2. Furthermore, JC-1 green fluorescence was significantly increased by ipragliflozin, suggesting the change of mitochondrial membrane potential. These findings suggest that the SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation via membrane hyperpolarization and mitochondrial membrane instability.Cancer is currently one of the major causes of death in patients with type 2 diabetes mellitus. We previously reported the beneficial effects of the glucagon-like peptide-1 receptor agonist exendin-4 against prostate and breast cancer. In the present study, we examined the anti-cancer effect of the sodium-glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin using a breast cancer model. In human breast cancer MCF-7 cells, SGLT2 expression was detected using both RT-PCR and immunohistochemistry. Ipragliflozin at 1-50 μM significantly and dose-dependently suppressed the growth of MCF-7 cells. BrdU assay also revealed that ipragliflozin attenuated the proliferation of MCF-7 cells in a dose-dependent manner. Because the effect of ipragliflozin against breast cancer cells was completely canceled by knocking down SGLT2, ipragliflozin could act via inhibiting SGLT2. We next measured membrane potential and whole-cell current using the patch clamp technique. When we treated MCF-7 cells with ipragliflozin or glucose-free medium, membrane hyperpolarization was observed. In addition, glucose-free medium and knockdown of SGLT2 by siRNA suppressed the glucose-induced whole-cell current of MCF-7 cells, suggesting that ipragliflozin inhibits sodium and glucose cotransport through SGLT2. Furthermore, JC-1 green fluorescence was significantly increased by ipragliflozin, suggesting the change of mitochondrial membrane potential. These findings suggest that the SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation via membrane hyperpolarization and mitochondrial membrane instability.
Author	Hamanoue, Nobuya Motonaga, Ryoko Nomiyama, Takashi Kawanami, Takako Tanabe, Makito Horikawa, Tsuyoshi Fujimura-Tanaka, Yuki Kawanami, Daiji Numata, Tomohiro Inoue, Ryuji Hamaguchi, Yuriko Komatsu, Shiho Yanase, Toshihiko Iwaya, Chikayo
Author_xml	– sequence: 1 fullname: Komatsu, Shiho organization: Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 2 fullname: Nomiyama, Takashi organization: Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 3 fullname: Numata, Tomohiro organization: Department of Physiology, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 4 fullname: Kawanami, Takako organization: Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 5 fullname: Hamaguchi, Yuriko organization: Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 6 fullname: Iwaya, Chikayo organization: Muta Hospital, Fukuoka, Japan – sequence: 7 fullname: Horikawa, Tsuyoshi organization: Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 8 fullname: Fujimura-Tanaka, Yuki organization: Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 9 fullname: Hamanoue, Nobuya organization: Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 10 fullname: Motonaga, Ryoko organization: Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 11 fullname: Tanabe, Makito organization: Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 12 fullname: Inoue, Ryuji organization: Department of Physiology, School of Medicine, Fukuoka University, Fukuoka, Japan – sequence: 13 fullname: Yanase, Toshihiko organization: Research Institute for Islet Biology, Fukuoka University, Fukuoka, Japan – sequence: 14 fullname: Kawanami, Daiji organization: Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/31776304$$D View this record in MEDLINE/PubMed
BookMark	eNp9kc1O3DAUhS1EBQPtA3RTReqmm1A7dvyzrBBMqUbqonRtOc4NeJSxB9tZtE-Pw0yDxKIbXy--c-_RORfo1AcPCH0k-Iq0WHwF3wcbt1c3P4iqMWvkCVoRymTNWoZP0QorImupWnWOLlLaYkxpy-gZOqdECE4xW6G7X-vNfVM5_-g6l0Os3D6ah9ENY_jrfGVyBj-ZDKnqIpiUK2u8hVhZGMdqH0MhIZrsgn-P3g1mTPDhOC_R79ub--vv9ebn-u7626a2XJFcq4FZJqgq05DGcswpbbhsCADrle2ZpMwazAg1g-pVGbwfaN91YJt-aIFeoi-HveX60wQp651Lsx3jIUxJN5QoJoUUbUE_v0G3YYq-uCsUU5JzhVWhPh2pqdtBr_fR7Uz8o_-FVAByAGwMKUUYFoRgPRehj0XouQg9F1E04o3GuvySU47Gjf9Vrg_K4sVZMwY_Og-vzu0TfxHpBjdYY8wFJhoTVr6qrCAlUMYJY-3rpm3K5gEW1yZmZ0dYbnOhyfwsHhbCPppYMPoM8i-_bw
CitedBy_id	crossref_primary_10_1007_s11033_024_09466_w crossref_primary_10_1016_j_jchf_2022_03_006 crossref_primary_10_1016_j_diabres_2023_110624 crossref_primary_10_32604_or_2024_048988 crossref_primary_10_1007_s10571_022_01221_8 crossref_primary_10_1007_s11154_021_09675_9 crossref_primary_10_1007_s13340_021_00494_6 crossref_primary_10_3390_ijms22041680 crossref_primary_10_3389_fphar_2024_1369352 crossref_primary_10_1007_s00210_024_03316_z crossref_primary_10_1038_s41419_022_04980_w crossref_primary_10_1016_j_phrs_2021_106039 crossref_primary_10_3390_biomedicines11071867 crossref_primary_10_1210_endocr_bqab079 crossref_primary_10_3389_fpubh_2021_668368 crossref_primary_10_3390_healthcare10071153 crossref_primary_10_1016_j_biopha_2020_110821 crossref_primary_10_3390_biom14111479 crossref_primary_10_3389_fphar_2024_1443045 crossref_primary_10_1016_j_jaccao_2024_08_001 crossref_primary_10_1016_j_ijcard_2023_131419 crossref_primary_10_3390_jpm13010157 crossref_primary_10_1016_j_ejphar_2024_176328 crossref_primary_10_1016_j_ejphar_2024_176803 crossref_primary_10_1093_eurheartj_ehab094 crossref_primary_10_1007_s10549_023_07024_9 crossref_primary_10_5114_aoms_174228 crossref_primary_10_1016_j_diabet_2023_101500 crossref_primary_10_3390_antiox10081166 crossref_primary_10_1016_j_jaccao_2024_01_007 crossref_primary_10_2478_fzm_2022_0030 crossref_primary_10_1186_s13098_024_01354_4 crossref_primary_10_3390_cancers16020299 crossref_primary_10_1002_mc_23837 crossref_primary_10_3390_hearts5040039 crossref_primary_10_2147_DDDT_S485755 crossref_primary_10_3390_cancers14235811 crossref_primary_10_1080_15384047_2024_2375440 crossref_primary_10_1002_cam4_5927 crossref_primary_10_2174_0113894501335877240926101134 crossref_primary_10_1007_s40264_023_01373_6 crossref_primary_10_1016_j_canlet_2021_07_035 crossref_primary_10_3390_molecules27217174 crossref_primary_10_1016_j_recesp_2024_07_004 crossref_primary_10_1038_s42003_022_03422_9 crossref_primary_10_1016_j_rec_2024_07_003 crossref_primary_10_1016_j_bioorg_2024_107214 crossref_primary_10_1080_17512433_2024_2439970 crossref_primary_10_3390_ijms21062164
Cites_doi	10.1007/s13340-011-0037-8 10.1038/s41598-018-19658-7 10.2337/db13-1169 10.1073/pnas.1511698112 10.3389/fonc.2019.00124 10.1007/s00125-017-4370-8 10.1507/endocrj.EJ18-0022 10.1007/s10549-016-3794-z 10.1038/bjc.1995.163 10.1056/NEJMoa1008862 10.2337/dc12-0336 10.1007/s00210-011-0713-z 10.1371/journal.pone.0139709 10.1507/endocrj.EJ15-0396 10.1210/en.2017-00461 10.1074/jbc.273.12.6951 10.1021/ja3007275 10.1007/s13340-013-0121-3
ContentType	Journal Article
Copyright	The Japan Endocrine Society Copyright Japan Science and Technology Agency 2020
Copyright_xml	– notice: The Japan Endocrine Society – notice: Copyright Japan Science and Technology Agency 2020
CorporateAuthor	Research Institute for Islet Biology Muta Hospital Department of Physiology School of Medicine Department of Endocrinology and Diabetes Mellitus Fukuoka University
CorporateAuthor_xml	– name: School of Medicine – name: Fukuoka University – name: Department of Endocrinology and Diabetes Mellitus – name: Department of Physiology – name: Muta Hospital – name: Research Institute for Islet Biology
DBID	AAYXX CITATION NPM 7QP 7T5 7TK 8FD FR3 H94 K9. NAPCQ P64 RC3 7X8
DOI	10.1507/endocrj.EJ19-0428
DatabaseName	CrossRef PubMed Calcium & Calcified Tissue Abstracts Immunology Abstracts Neurosciences Abstracts Technology Research Database Engineering Research Database AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) Nursing & Allied Health Premium Biotechnology and BioEngineering Abstracts Genetics Abstracts MEDLINE - Academic
DatabaseTitle	CrossRef PubMed Nursing & Allied Health Premium Genetics Abstracts Technology Research Database AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) Immunology Abstracts Engineering Research Database Calcium & Calcified Tissue Abstracts Neurosciences Abstracts Biotechnology and BioEngineering Abstracts MEDLINE - Academic
DatabaseTitleList	Nursing & Allied Health Premium MEDLINE - Academic PubMed
Database_xml	– sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database
DeliveryMethod	fulltext_linktorsrc
Discipline	Medicine
EISSN	1348-4540
EndPage	106
ExternalDocumentID	31776304 10_1507_endocrj_EJ19_0428 cq6endoc_2020_006701_014_0099_01063461445 article_endocrj_67_1_67_EJ19_0428_article_char_en
Genre	Journal Article
GroupedDBID	--- .55 .GJ 29G 2WC 3O- 53G 5GY 5RE AAEJM AAUGY ACPRK ACRZS ADBBV AENEX AJJEV ALMA_UNASSIGNED_HOLDINGS BAWUL BKOMP CS3 DIK DU5 E3Z EBD EBS EJD EMOBN F5P JMI JSF JSH KQ8 MOJWN M~E OK1 P2P RJT RNS RZJ SV3 TKC TR2 X7M XSB ZGI ZXP AAFWJ AFPKN GROUPED_DOAJ OVT RPM AAYXX CITATION NPM 7QP 7T5 7TK 8FD FR3 H94 K9. NAPCQ P64 RC3 7X8
ID	FETCH-LOGICAL-c691t-9f4c47399f4a12c6063326821ee4d9cd4834ca0413af9d913a6df3dbbec2df5e3
ISSN	0918-8959 1348-4540
IngestDate	Fri Jul 11 01:21:31 EDT 2025 Mon Jun 30 07:48:47 EDT 2025 Thu Jan 02 22:59:43 EST 2025 Tue Jul 01 01:17:31 EDT 2025 Thu Apr 24 23:10:50 EDT 2025 Thu Jul 10 16:10:47 EDT 2025 Thu Aug 17 20:30:00 EDT 2023
IsDoiOpenAccess	true
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	1
Keywords	Mitochondria Breast cancer Membrane potential SGLT2 inhibitor
Language	English
LinkModel	OpenURL
MergedId	FETCHMERGED-LOGICAL-c691t-9f4c47399f4a12c6063326821ee4d9cd4834ca0413af9d913a6df3dbbec2df5e3
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23
OpenAccessLink	https://www.jstage.jst.go.jp/article/endocrj/67/1/67_EJ19-0428/_article/-char/en
PMID	31776304
PQID	2349866909
PQPubID	2048504
PageCount	8
ParticipantIDs	proquest_miscellaneous_2319487875 proquest_journals_2349866909 pubmed_primary_31776304 crossref_primary_10_1507_endocrj_EJ19_0428 crossref_citationtrail_10_1507_endocrj_EJ19_0428 medicalonline_journals_cq6endoc_2020_006701_014_0099_01063461445 jstage_primary_article_endocrj_67_1_67_EJ19_0428_article_char_en
ProviderPackageCode	CITATION AAYXX
PublicationCentury	2000
PublicationDate	2020-01-01
PublicationDateYYYYMMDD	2020-01-01
PublicationDate_xml	– month: 01 year: 2020 text: 2020-01-01 day: 01
PublicationDecade	2020
PublicationPlace	Japan
PublicationPlace_xml	– name: Japan – name: Kyoto
PublicationTitle	ENDOCRINE JOURNAL
PublicationTitleAlternate	Endocr J
PublicationYear	2020
Publisher	The Japan Endocrine Society Japan Science and Technology Agency
Publisher_xml	– name: The Japan Endocrine Society – name: Japan Science and Technology Agency
References	5 Iwaya C, Nomiyama T, Komatsu S, Kawanami T, Tsutsumi Y, et al. (2017) Exendin-4, a glucagonlike peptide-1 receptor agonist, attenuates breast cancer growth by inhibiting NF-kB activation. Endocrinology 158: 4218–4232. 2 Kasuga M, Ueki K, Tajima N, Noda M, Ohashi K, et al. (2013) Report of the JDS/JCA joint committee on diabetes and cancer. Diabetol Int 4: 81–96. 11 Scafoglio C, Hirayama BA, Kepe V, Liu J, Ghezzi C, et al. (2015) Functional expression of sodium-glucose transporters in cancer. Proc Natl Acad Sci USA 112: E4111–E4119. 20 Okada J, Matsumoto S, Kaira K, Saito T, Saito T, et al. (2018) Sodium glucose cotransporter 2 inhibition combined with cetuximab significantly reduced tumor size and carcinoembryonic antigen level in colon cancer metastatic to liver. Clin Colorectal Cancer 17: e45–e48. 12 Shiba K, Tsuchiya K, Komiya C, Miyachi Y, Mori K, et al. (2018) Canagliflozin, an SGLT2 inhibitor, attenuates the development of hepatocellular carcinoma in a mouse model of human NASH. Sci Rep 8: 2362. 17 Numata M, Petrecca K, Lake N, Orlowski J (1998) Identification of a mitochondrial Na+/H+ exchanger. J Biol Chem 273: 6951–6959. 7 Tahara A, Kurosaki E, Yokono M, Yamajuku D, Kihara R, et al. (2012) Pharmacological profile of ipragliflozin (ASP1941), a novel selective SGLT2 inhibitor, in vitro and in vivo. Naunyn Schmiedebergs Arch Pharmacol 385: 423–436. 8 Nomiyama T, Shimono D, Horikawa T, Fujimura Y, Ohsako T, et al. (2018) Efficacy and safety of sodium-glucose cotransporter 2 inhibitor ipragliflozin on glycemic control and cardiovascular parameters in Japanese patients with type 2 diabetes mellitus; Fukuoka Study of Ipragliflozin (FUSION). Endocr J 65: 859–867. 18 Martel F, Guedes M, Keating E (2016) Effect of polyphenols on glucose and lactate transport by breast cancer cell. Breast Cancer Res Treat 157: 1–11. 14 Kadokura T, Saito M, Utsuno A, Kazuta K, Yoshida S, et al. (2011) Ipragliflozin (ASP1941), a selective sodium-dependent glucose cotransporter 2 inhibitor, safely stimulates urinaly glucose excretion without inducing hypoglycemia in healthy Japanese Subjects. Diabetol Int 2: 172–182. 6 Tsutsumi Y, Nomiyama T, Kawanami T, Hamagichi Y, Terawaki Y, et al. (2015) Combined treatment with Exendin-4 and metformin attenuates prostate cancer growth. PLoS One 10: e0139709 9 Kurebayashi J, Kurosumi M, Sonoo H (1995) A new human breast cancer cell line, KPL-1 secretes tumor-associated antigens and grows rapidly in female athymic nude mice. Br J Cancer 71: 845–853. 10 Numata T, Murakami T, Kawashima F, Moroue N, Heuser JF, et al. (2012) Utilization of photoinduced charge-separated state of donor-acceptor-linked molecules for regulation of cell membrane potential and ion transport. J Am Chem Soc 134: 6092–6095. 13 Saito T, Okada S, Yamada E, Shimoda Y, Osaki A, et al. (2015) Effect of dapagliflozin on colon cancer cell. Endocr J 62: 1133–1137. 15 Mao W, Zhang J, Komer H, Jiang Y, Ying S (2019) The emerging role of voltage-gated sodium channels in tumor biology. Front Oncol 9: 124. 19 Tang H, Dai Q, Shi W, Zhai S, Song Y, et al. (2017) SGLT2 inhibitors and risk of cancer in type 2 diabetes: a systematic review and meta-analysis of randomised control trials. Diabetologia 60: 1862–1872. 16 Baysal K, Jung DW, Gunter KK, Gunter TE, Brierley GP (1994) Na(+)-dependent Ca2+ efflux mechanism of heart mitochondria is not a positive Ca2+/2Na+ exchanger. Am J Physiol 266: C800–C808. 1 Emerging Risk Factors Collaboration, Seshasai SR, Kaptoqe S, Thompson A, Di Angelantonio E, Gao P, et al. (2011) Diabetes mellitus, fasting glucose, and risk of cause-specific death. N Engl J Med 364: 829–841. 3 Esposito K, Chiodini P, Colao A, Lenzi A, Giugliano D (2012) Metabolic syndrome and risk of cancer: a systemic review and meta-analysis. Diabetes Care 35: 2402–2411. 4 Nomiyama T, Kawanami T, Irie S, Hamaguchi Y, Terawaki Y, et al. (2014) Exendin-4, a glicagon-like peptide-1 receptor agonist, attenuates prostate cancer growth. Diabetes 63: 3891–3905. 11 K Esposito (3) 2012; 35 12 13 14 15 16 17 18 19 1 2 4 5 6 7 8 9 20 10
References_xml	– reference: 4 Nomiyama T, Kawanami T, Irie S, Hamaguchi Y, Terawaki Y, et al. (2014) Exendin-4, a glicagon-like peptide-1 receptor agonist, attenuates prostate cancer growth. Diabetes 63: 3891–3905. – reference: 8 Nomiyama T, Shimono D, Horikawa T, Fujimura Y, Ohsako T, et al. (2018) Efficacy and safety of sodium-glucose cotransporter 2 inhibitor ipragliflozin on glycemic control and cardiovascular parameters in Japanese patients with type 2 diabetes mellitus; Fukuoka Study of Ipragliflozin (FUSION). Endocr J 65: 859–867. – reference: 17 Numata M, Petrecca K, Lake N, Orlowski J (1998) Identification of a mitochondrial Na+/H+ exchanger. J Biol Chem 273: 6951–6959. – reference: 7 Tahara A, Kurosaki E, Yokono M, Yamajuku D, Kihara R, et al. (2012) Pharmacological profile of ipragliflozin (ASP1941), a novel selective SGLT2 inhibitor, in vitro and in vivo. Naunyn Schmiedebergs Arch Pharmacol 385: 423–436. – reference: 20 Okada J, Matsumoto S, Kaira K, Saito T, Saito T, et al. (2018) Sodium glucose cotransporter 2 inhibition combined with cetuximab significantly reduced tumor size and carcinoembryonic antigen level in colon cancer metastatic to liver. Clin Colorectal Cancer 17: e45–e48. – reference: 15 Mao W, Zhang J, Komer H, Jiang Y, Ying S (2019) The emerging role of voltage-gated sodium channels in tumor biology. Front Oncol 9: 124. – reference: 2 Kasuga M, Ueki K, Tajima N, Noda M, Ohashi K, et al. (2013) Report of the JDS/JCA joint committee on diabetes and cancer. Diabetol Int 4: 81–96. – reference: 18 Martel F, Guedes M, Keating E (2016) Effect of polyphenols on glucose and lactate transport by breast cancer cell. Breast Cancer Res Treat 157: 1–11. – reference: 6 Tsutsumi Y, Nomiyama T, Kawanami T, Hamagichi Y, Terawaki Y, et al. (2015) Combined treatment with Exendin-4 and metformin attenuates prostate cancer growth. PLoS One 10: e0139709 – reference: 5 Iwaya C, Nomiyama T, Komatsu S, Kawanami T, Tsutsumi Y, et al. (2017) Exendin-4, a glucagonlike peptide-1 receptor agonist, attenuates breast cancer growth by inhibiting NF-kB activation. Endocrinology 158: 4218–4232. – reference: 3 Esposito K, Chiodini P, Colao A, Lenzi A, Giugliano D (2012) Metabolic syndrome and risk of cancer: a systemic review and meta-analysis. Diabetes Care 35: 2402–2411. – reference: 14 Kadokura T, Saito M, Utsuno A, Kazuta K, Yoshida S, et al. (2011) Ipragliflozin (ASP1941), a selective sodium-dependent glucose cotransporter 2 inhibitor, safely stimulates urinaly glucose excretion without inducing hypoglycemia in healthy Japanese Subjects. Diabetol Int 2: 172–182. – reference: 19 Tang H, Dai Q, Shi W, Zhai S, Song Y, et al. (2017) SGLT2 inhibitors and risk of cancer in type 2 diabetes: a systematic review and meta-analysis of randomised control trials. Diabetologia 60: 1862–1872. – reference: 11 Scafoglio C, Hirayama BA, Kepe V, Liu J, Ghezzi C, et al. (2015) Functional expression of sodium-glucose transporters in cancer. Proc Natl Acad Sci USA 112: E4111–E4119. – reference: 16 Baysal K, Jung DW, Gunter KK, Gunter TE, Brierley GP (1994) Na(+)-dependent Ca2+ efflux mechanism of heart mitochondria is not a positive Ca2+/2Na+ exchanger. Am J Physiol 266: C800–C808. – reference: 10 Numata T, Murakami T, Kawashima F, Moroue N, Heuser JF, et al. (2012) Utilization of photoinduced charge-separated state of donor-acceptor-linked molecules for regulation of cell membrane potential and ion transport. J Am Chem Soc 134: 6092–6095. – reference: 13 Saito T, Okada S, Yamada E, Shimoda Y, Osaki A, et al. (2015) Effect of dapagliflozin on colon cancer cell. Endocr J 62: 1133–1137. – reference: 1 Emerging Risk Factors Collaboration, Seshasai SR, Kaptoqe S, Thompson A, Di Angelantonio E, Gao P, et al. (2011) Diabetes mellitus, fasting glucose, and risk of cause-specific death. N Engl J Med 364: 829–841. – reference: 9 Kurebayashi J, Kurosumi M, Sonoo H (1995) A new human breast cancer cell line, KPL-1 secretes tumor-associated antigens and grows rapidly in female athymic nude mice. Br J Cancer 71: 845–853. – reference: 12 Shiba K, Tsuchiya K, Komiya C, Miyachi Y, Mori K, et al. (2018) Canagliflozin, an SGLT2 inhibitor, attenuates the development of hepatocellular carcinoma in a mouse model of human NASH. Sci Rep 8: 2362. – ident: 14 doi: 10.1007/s13340-011-0037-8 – ident: 12 doi: 10.1038/s41598-018-19658-7 – ident: 4 doi: 10.2337/db13-1169 – ident: 11 doi: 10.1073/pnas.1511698112 – ident: 15 doi: 10.3389/fonc.2019.00124 – ident: 19 doi: 10.1007/s00125-017-4370-8 – ident: 8 doi: 10.1507/endocrj.EJ18-0022 – ident: 16 – ident: 18 doi: 10.1007/s10549-016-3794-z – ident: 9 doi: 10.1038/bjc.1995.163 – ident: 1 doi: 10.1056/NEJMoa1008862 – volume: 35 start-page: 2402 issn: 0149-5992 year: 2012 ident: 3 publication-title: Diabetes Care doi: 10.2337/dc12-0336 – ident: 7 doi: 10.1007/s00210-011-0713-z – ident: 6 doi: 10.1371/journal.pone.0139709 – ident: 13 doi: 10.1507/endocrj.EJ15-0396 – ident: 5 doi: 10.1210/en.2017-00461 – ident: 17 doi: 10.1074/jbc.273.12.6951 – ident: 10 doi: 10.1021/ja3007275 – ident: 20 – ident: 2 doi: 10.1007/s13340-013-0121-3
SSID	ssj0033543 ssib022572652 ssib044735826 ssib058492669 ssib002822051 ssib000750009
Score	2.4723127
Snippet	Cancer is currently one of the major causes of death in patients with type 2 diabetes mellitus. We previously reported the beneficial effects of the... [Abstract.] Cancer is currently one of the major causes of death in patients with type 2 diabetes mellitus. We previously reported the beneficial effects of...
SourceID	proquest pubmed crossref medicalonline jstage
SourceType	Aggregation Database Index Database Enrichment Source Publisher
StartPage	99
SubjectTerms	Breast cancer Cell growth Cell proliferation Diabetes mellitus (non-insulin dependent) Glucagon Glucagon-like peptide 1 Glucose Hyperpolarization Immunohistochemistry Membrane potential Mitochondria Na+/glucose cotransporter Polymerase chain reaction Prostate cancer SGLT2 inhibitor siRNA
Title	SGLT2 inhibitor ipragliflozin attenuates breast cancer cell proliferation
URI	https://www.jstage.jst.go.jp/article/endocrj/67/1/67_EJ19-0428/_article/-char/en http://mol.medicalonline.jp/en/journal/download?GoodsID=cq6endoc/2020/006701/014&name=0099-0106e https://www.ncbi.nlm.nih.gov/pubmed/31776304 https://www.proquest.com/docview/2349866909 https://www.proquest.com/docview/2319487875
Volume	67
hasFullText	1
inHoldings	1
isFullTextHit
isPrint
ispartofPNX	Endocrine Journal, 2020, Vol.67(1), pp.99-106
link	http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3db9MwELfKQAgJIb4pDBQknogy8uG48RsIDcbGkBCdtDcrsR2arU1G1wox_nnu7MRtGEOMF7dK7FPi-8jP57szIS_KMlEqVjpgUrOAYgBhEWkdKFaknGUJY2b3fP8T2zmgu4fp4WDwcz27ZFFsybM_5pX8D1fhGvAVs2QvwVlHFC7Af-AvtMBhaP-Jx1_efxzHflVPqgIUc-5XJ_P867Qqp81ZVftYObNeIpb0Cww9X2CEl9RzH531GJg1xbCWFWc6_3ytGok5gf76M5jsGEC3p0vjL51Uk8b5kZtZ9SOfGRQ6zo_xdCZ3awlD7I1m1kyquRu0l3_P63xWdYOOm3X_Qxyu-R9aR2KUBRlv63pra0YTdFOmthBTZ2ftsRs9ebJGk_O1z29kChCct-ypCebQZgqOtrZ3MfeKtnnlvSrav33dXMwhrnaAiGhJCCQhkMQVcjWGNQYayb3PbgsqSVIbctm9XrslDiRenXuKHqi5dgS4Hgs23JzZvTZb8-TiJYyBMuPb5Fa7BvHeWIG6Qwa6vkuu77dRFvfIByNXnpMrrydX3kquPCtXnpUrD-XK68nVfXLwbnv8didoj9wIJOPRIuAllXQEoLWkeRRLWN0mgO-zGNSXKi4Vup5lHgLyyUuuOPwwBdpegCWIVZnq5AHZqJtaPyKeSlhajAqG8IdSzTOZqgigkdJqpIqYDknYzZmQbT16PBZlKi7k1JC8dENObDGWv3V-bRnhurZ66rqykYiwcUNcD8x4hG5AosdC0erdqZDfmKEiUCOESXaLRBhRgSsugX6WhKKrJR2SzY7rq9FxQnkGVjDkQ_Lc3Qa7jnzKa90ssU_EaQafUyDx0EqLexHA_AALQvr4MvPxhNxYqe8m2VjMl_opAOpF8cwI_i915c6G
linkProvider	Colorado Alliance of Research Libraries
openUrl	ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=SGLT2+inhibitor+ipragliflozin+attenuates+breast+cancer+cell+proliferation&rft.jtitle=Endocrine+journal&rft.au=Komatsu%2C+Shiho&rft.au=Nomiyama%2C+Takashi&rft.au=Numata%2C+Tomohiro&rft.au=Kawanami%2C+Takako&rft.date=2020-01-01&rft.issn=0918-8959&rft.eissn=1348-4540&rft.volume=67&rft.issue=1&rft.spage=99&rft.epage=106&rft_id=info:doi/10.1507%2Fendocrj.EJ19-0428&rft.externalDBID=n%2Fa&rft.externalDocID=10_1507_endocrj_EJ19_0428
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0918-8959&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0918-8959&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0918-8959&client=summon