Endogenous tumor necrosis factor inhibits the cytotoxicity of exogenous tumor necrosis factor and adriamycin in pancreatic carcinoma cells
Pancreatic carcinoma is one of the most devastating neoplasms with regard to its resistance to conventional therapy. In a previous report, we found that endogenous tumor necrosis factor (enTNF) exerts an intracellular protective effect against exogenous TNF- and Adriamycin (ADM)-induced cytotoxicity...
Saved in:
Published in | Pancreas Vol. 13; no. 4; p. 395 |
---|---|
Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.11.1996
|
Subjects | |
Online Access | Get more information |
Cover
Loading…
Abstract | Pancreatic carcinoma is one of the most devastating neoplasms with regard to its resistance to conventional therapy. In a previous report, we found that endogenous tumor necrosis factor (enTNF) exerts an intracellular protective effect against exogenous TNF- and Adriamycin (ADM)-induced cytotoxicity by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD). We also know that glutathione S-transferase pi (GST-pi) and glutathione (GSH) also scavenge OFR. It remains unclear to what extent enTNF and MnSOD induced by enTNF regulate the sensitivity to ADM and exogenous TNF among different carcinoma cells. In this study, we examined the relationship between ADM and exogenous TNF sensitivity and en-TNF expression and MnSOD activity in four pancreatic carcinoma lines. We determined whether ADM and exogenous TNF sensitivity could be predicted by measuring enTNF expression and MnSOD activity in the carcinoma cells. The sensitivity to TNF and ADM varied with the cell lines, and TNF sensitivity correlated well with Adriamycin sensitivity. Moreover, enTNF expression and Mn-SOD activity correlated positively with resistance to ADM and exogenous TNF. When MIAPaCa-2 cells, which had the lowest enTNF expression and the highest sensitivity to exogenous TNF and ADM, were transfected with the nonsecretory-type human TNF gene (pTNF delta pro) to increase enTNF synthesis, their intracellular MnSOD activity and exogenous TNF and ADM resistance were increased. These findings suggest that MnSOD plays a critical role in scavenging OFR induced by ADM and exogenous TNF. enTNF is the most important factor that regulates the production of MnSOD. Therefore, it is plausible that inhibition of enTNF expression or MnSOD activity in pancreatic carcinoma would improve the efficacy of therapies for pancreatic carcinoma. |
---|---|
AbstractList | Pancreatic carcinoma is one of the most devastating neoplasms with regard to its resistance to conventional therapy. In a previous report, we found that endogenous tumor necrosis factor (enTNF) exerts an intracellular protective effect against exogenous TNF- and Adriamycin (ADM)-induced cytotoxicity by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD). We also know that glutathione S-transferase pi (GST-pi) and glutathione (GSH) also scavenge OFR. It remains unclear to what extent enTNF and MnSOD induced by enTNF regulate the sensitivity to ADM and exogenous TNF among different carcinoma cells. In this study, we examined the relationship between ADM and exogenous TNF sensitivity and en-TNF expression and MnSOD activity in four pancreatic carcinoma lines. We determined whether ADM and exogenous TNF sensitivity could be predicted by measuring enTNF expression and MnSOD activity in the carcinoma cells. The sensitivity to TNF and ADM varied with the cell lines, and TNF sensitivity correlated well with Adriamycin sensitivity. Moreover, enTNF expression and Mn-SOD activity correlated positively with resistance to ADM and exogenous TNF. When MIAPaCa-2 cells, which had the lowest enTNF expression and the highest sensitivity to exogenous TNF and ADM, were transfected with the nonsecretory-type human TNF gene (pTNF delta pro) to increase enTNF synthesis, their intracellular MnSOD activity and exogenous TNF and ADM resistance were increased. These findings suggest that MnSOD plays a critical role in scavenging OFR induced by ADM and exogenous TNF. enTNF is the most important factor that regulates the production of MnSOD. Therefore, it is plausible that inhibition of enTNF expression or MnSOD activity in pancreatic carcinoma would improve the efficacy of therapies for pancreatic carcinoma. |
Author | Yamauchi, N Sasaki, H Okamoto, T Akiyama, S Watanabe, N Kobayashi, D Sato, T Tsuji, N Tsuji, Y Niitsu, Y |
Author_xml | – sequence: 1 givenname: N surname: Watanabe fullname: Watanabe, N organization: Fourth Department of Internal Medicine, Sapporo Medical University, School of Medicine, Japan – sequence: 2 givenname: N surname: Tsuji fullname: Tsuji, N – sequence: 3 givenname: Y surname: Tsuji fullname: Tsuji, Y – sequence: 4 givenname: H surname: Sasaki fullname: Sasaki, H – sequence: 5 givenname: T surname: Okamoto fullname: Okamoto, T – sequence: 6 givenname: S surname: Akiyama fullname: Akiyama, S – sequence: 7 givenname: D surname: Kobayashi fullname: Kobayashi, D – sequence: 8 givenname: T surname: Sato fullname: Sato, T – sequence: 9 givenname: N surname: Yamauchi fullname: Yamauchi, N – sequence: 10 givenname: Y surname: Niitsu fullname: Niitsu, Y |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/8899800$$D View this record in MEDLINE/PubMed |
BookMark | eNp9kE1qwzAQhbVISZO0RyjoAm4l2_qZZQnpDwS6addBHsmNSiwFS4H4Cj11VZp1ZzO895gP5i3JLMTgCKGc3XMG6oGVkVLJigNIzouqfi2YkQXTWlQNV-qaLFP6YoyrRsCczLUG0IwtyPcm2PjpQjwlmk9DHGlwOMbkE-0N5qJ92PvO5xLvHcUpxxzPHn2eaOypO_9_bIKlxo7eDBP6UFj0aAKOzmSPFM1YzDgYiu5wSDfkqjeH5G4ve0U-njbv65dq-_b8un7cVtgylSsFqLnuQSJrLG_AYg8NZ5yJpnzdMu6gVTV2iCBqKa10hqMTIABa0emuXpG7P-7x1A3O7o6jH8w47S6d1D9a7WhZ |
CitedBy_id | crossref_primary_10_1053_gast_2001_23627 crossref_primary_10_1081_DMR_200033488 crossref_primary_10_1371_journal_pone_0077126 crossref_primary_10_1111_j_1349_7006_2001_tb01189_x crossref_primary_10_3109_02656739809018235 crossref_primary_10_1097_00006676_200203000_00007 crossref_primary_10_1054_bjoc_2001_1954 crossref_primary_10_1016_j_tox_2008_02_018 crossref_primary_10_1074_jbc_M208665200 crossref_primary_10_3109_10428199909083376 crossref_primary_10_1097_mpa_0b013e31814dadf5 crossref_primary_10_1158_0008_5472_CAN_07_5704 crossref_primary_10_1111_j_1349_7006_2000_tb00906_x crossref_primary_10_1002__SICI_1097_0215_19980518_76_4_552__AID_IJC18_3_0_CO_2_9 crossref_primary_10_1248_bpb_b13_00121 crossref_primary_10_1593_neo_06646 crossref_primary_10_1073_pnas_0611660104 |
ContentType | Journal Article |
DBID | CGR CUY CVF ECM EIF NPM |
DOI | 10.1097/00006676-199611000-00009 |
DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed |
DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) |
DatabaseTitleList | MEDLINE |
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 – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
DeliveryMethod | no_fulltext_linktorsrc |
Discipline | Medicine |
ExternalDocumentID | 8899800 |
Genre | Journal Article |
GroupedDBID | --- .-D .55 .GJ .XZ .Z2 0R~ 123 4Q1 4Q2 4Q3 53G 5RE 5VS 8L- AAAAV AAHPQ AAIQE AAJCS AAMTA AARTV AASCR AAYEP ABASU ABBUW ABDIG ABJNI ABOCM ABVCZ ABXVJ ABZAD ACCJW ACDDN ACEWG ACGFO ACGFS ACILI ACWDW ACWRI ACXJB ACXNZ ADFPA ADGGA ADHPY ADNKB AE3 AE6 AEBDS AEETU AENEX AFDTB AFEXH AFUWQ AHQNM AHRYX AHVBC AINUH AJIOK AJNWD AJNYG AJZMW ALMA_UNASSIGNED_HOLDINGS ALMTX AMJPA AMKUR AMNEI AOHHW AWKKM BQLVK BS7 C45 CGR CS3 CUY CVF DIWNM DU5 DUNZO E.X EBS ECM EEVPB EIF EJD EX3 F2K F2L F5P FCALG FL- GNXGY GQDEL H0~ HLJTE HZ~ IKREB IN~ JF9 JG8 JK3 JK8 K8S KD2 KMI L-C N9A NPM N~M O9- OAG OAH OCUKA ODA ODMTH OHYEH OJAPA OL1 OLG OLV OLW OLZ OPUJH ORVUJ OUVQU OVD OVDNE OWU OWV OWW OWX OWY OWZ OXXIT P-K P2P R58 RLZ S4R S4S T8P TEORI TSPGW V2I VVN W3M WOQ WOW X3V X3W X7M XXN XYM YFH ZFV ZXP ZZMQN |
ID | FETCH-LOGICAL-c407t-79c818f96c03d139dcf93101053000401e9472cbcc95266d6ea1ce5959945b8b2 |
ISSN | 0885-3177 |
IngestDate | Sat Sep 28 08:39:34 EDT 2024 |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 4 |
Language | English |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c407t-79c818f96c03d139dcf93101053000401e9472cbcc95266d6ea1ce5959945b8b2 |
PMID | 8899800 |
ParticipantIDs | pubmed_primary_8899800 |
PublicationCentury | 1900 |
PublicationDate | 1996-11-01 |
PublicationDateYYYYMMDD | 1996-11-01 |
PublicationDate_xml | – month: 11 year: 1996 text: 1996-11-01 day: 01 |
PublicationDecade | 1990 |
PublicationPlace | United States |
PublicationPlace_xml | – name: United States |
PublicationTitle | Pancreas |
PublicationTitleAlternate | Pancreas |
PublicationYear | 1996 |
SSID | ssj0017359 |
Score | 1.6089362 |
Snippet | Pancreatic carcinoma is one of the most devastating neoplasms with regard to its resistance to conventional therapy. In a previous report, we found that... |
SourceID | pubmed |
SourceType | Index Database |
StartPage | 395 |
SubjectTerms | Doxorubicin - therapeutic use Drug Resistance, Neoplasm Gene Expression Humans Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - enzymology Superoxide Dismutase - metabolism Transfection Tumor Cells, Cultured Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - pharmacology Tumor Necrosis Factor-alpha - therapeutic use |
Title | Endogenous tumor necrosis factor inhibits the cytotoxicity of exogenous tumor necrosis factor and adriamycin in pancreatic carcinoma cells |
URI | https://www.ncbi.nlm.nih.gov/pubmed/8899800 |
Volume | 13 |
hasFullText | |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Na9wwEBWbhpRcStM29Bsdcltc7Ei2rGMpKaGQEMiG5hasL-LC2qHrhaQ_oZf-5c5IstdNNqHtxSzSWqw9b0dvpNEbQvY4Fw5mGpswk5cQoFiTVA6iFJ2x0jCpjZB4GvnouDg841_O8_PJ5Ncoa2nZqQ_6x9pzJf9jVWgDu-Ip2X-w7DAoNMBnsC9cwcJw_SsbHzSmjSKr3XLefp82Fme9ehHL6Ezr5rJWuDWA9FLfdG3XXtc6ZmHY64dv9jKuBh5jfqNrnxAJniOQTI2K1tDYzqspLv0vxhz3JHxrIOtfKyCglbJ_bPzMFstv9fqWgVyfVotqVFU7LE74fOZsWJzofRhutMdKLb3DZSNg8ZH3ZKHe5h2vHtSC_dRaiAJzYwpUuvNH4r24Qjcy9tXcW7vEQNKLoD7ceUttO_ZskA1RosM8xsWfuCklmK-9NzxTTAzrNUDX_bZtshVHvBW2ePoye0qexLiDfgwg2iET2zwjj49iZsVz8nOFJerhQHs40AAH2mOJApboGEu0dXTA0j03A5boCkswFl1hiQ5Yoh5LL8jZ54PZp8Mk1ulINE9FlwipgfY5WeiUGYgojHYSogZg7gxDhjSzkot9rbSWOfBBU9gqw9N_uZQ8V6Xa3yWPmraxLwmtgF1yzGxWmeKpK8rUoSCcFs6w3OjsFdkNb_HiKoixXMTX-_q-jjdkewXMt2TTwX_fvgMi2an33ry_AdRec-A |
link.rule.ids | 786 |
linkProvider | National Library of Medicine |
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=Endogenous+tumor+necrosis+factor+inhibits+the+cytotoxicity+of+exogenous+tumor+necrosis+factor+and+adriamycin+in+pancreatic+carcinoma+cells&rft.jtitle=Pancreas&rft.au=Watanabe%2C+N&rft.au=Tsuji%2C+N&rft.au=Tsuji%2C+Y&rft.au=Sasaki%2C+H&rft.date=1996-11-01&rft.issn=0885-3177&rft.volume=13&rft.issue=4&rft.spage=395&rft_id=info:doi/10.1097%2F00006676-199611000-00009&rft_id=info%3Apmid%2F8899800&rft_id=info%3Apmid%2F8899800&rft.externalDocID=8899800 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0885-3177&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0885-3177&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0885-3177&client=summon |