Long noncoding RNA LINC00152 promotes cell proliferation through competitively binding endogenous miR‐125b with MCL‐1 by regulating mitochondrial apoptosis pathways in ovarian cancer
Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA expression was found to relate to the development and pathogenesis of multiple cancers. LncRNA LINC00152 served as an oncogene in multiple cancers; howe...
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| Published in | Cancer medicine (Malden, MA) Vol. 7; no. 9; pp. 4530 - 4541 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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United States
John Wiley & Sons, Inc
01.09.2018
John Wiley and Sons Inc Wiley |
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| Abstract | Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA expression was found to relate to the development and pathogenesis of multiple cancers. LncRNA LINC00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC00152 and Myeloid cell leukemia‐1 (MCL‐1) were targeted by miR‐125b and had the same miR‐125b combining site. The miR‐125b level was negatively correlated with the expression of LINC00152, while MCL‐1 was positively related to the LINC00152 level. MiR‐125b could affect LINC00152 levels as evaluated by qRT‐PCR. Finally, we affirmed that LINC00152 mediated cell proliferation by affecting MCL‐1 expression and MCL‐1‐mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ceRNA) of miR‐125b. In summary, based on ceRNA theory, the combined research on miR‐125b and MCL‐1, and taking LINC00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer.
LINC00152 is upregulated in ovarian cancer tissues and cell lines. LINC00152 is a target of miR‐125b and modulates its target MCL‐1. LINC00152/miR‐125b/MCL‐1 axis modulated mitochondrial apoptosis pathway on cell apoptosis in ovarian cancer cells. |
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| AbstractList | Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA expression was found to relate to the development and pathogenesis of multiple cancers. LncRNA LINC00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC00152 and Myeloid cell leukemia-1 (MCL-1) were targeted by miR-125b and had the same miR-125b combining site. The miR-125b level was negatively correlated with the expression of LINC00152, while MCL-1 was positively related to the LINC00152 level. MiR-125b could affect LINC00152 levels as evaluated by qRT-PCR. Finally, we affirmed that LINC00152 mediated cell proliferation by affecting MCL-1 expression and MCL-1-mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ceRNA) of miR-125b. In summary, based on ceRNA theory, the combined research on miR-125b and MCL-1, and taking LINC00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer. Recently, an increasing number of studies have focused on the key function of long noncoding RNA s (lnc RNA s) in biological activity. Abnormal lnc RNA expression was found to relate to the development and pathogenesis of multiple cancers. Lnc RNA LINC 00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC 00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC 00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC 00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC 00152 and Myeloid cell leukemia‐1 ( MCL ‐1) were targeted by miR‐125b and had the same miR‐125b combining site. The miR‐125b level was negatively correlated with the expression of LINC 00152, while MCL ‐1 was positively related to the LINC 00152 level. MiR‐125b could affect LINC 00152 levels as evaluated by qRT ‐ PCR . Finally, we affirmed that LINC 00152 mediated cell proliferation by affecting MCL ‐1 expression and MCL ‐1‐mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ce RNA ) of miR‐125b. In summary, based on ce RNA theory, the combined research on miR‐125b and MCL ‐1, and taking LINC 00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer. Abstract Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA expression was found to relate to the development and pathogenesis of multiple cancers. LncRNA LINC00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC00152 and Myeloid cell leukemia‐1 (MCL‐1) were targeted by miR‐125b and had the same miR‐125b combining site. The miR‐125b level was negatively correlated with the expression of LINC00152, while MCL‐1 was positively related to the LINC00152 level. MiR‐125b could affect LINC00152 levels as evaluated by qRT‐PCR. Finally, we affirmed that LINC00152 mediated cell proliferation by affecting MCL‐1 expression and MCL‐1‐mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ceRNA) of miR‐125b. In summary, based on ceRNA theory, the combined research on miR‐125b and MCL‐1, and taking LINC00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer. Recently, an increasing number of studies have focused on the key function of long noncoding RNA s (lnc RNA s) in biological activity. Abnormal lnc RNA expression was found to relate to the development and pathogenesis of multiple cancers. Lnc RNA LINC 00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC 00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC 00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC 00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC 00152 and Myeloid cell leukemia‐1 ( MCL ‐1) were targeted by miR‐125b and had the same miR‐125b combining site. The miR‐125b level was negatively correlated with the expression of LINC 00152, while MCL ‐1 was positively related to the LINC 00152 level. MiR‐125b could affect LINC 00152 levels as evaluated by qRT ‐ PCR . Finally, we affirmed that LINC 00152 mediated cell proliferation by affecting MCL ‐1 expression and MCL ‐1‐mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ce RNA ) of miR‐125b. In summary, based on ce RNA theory, the combined research on miR‐125b and MCL ‐1, and taking LINC 00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer. Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA expression was found to relate to the development and pathogenesis of multiple cancers. LncRNA LINC00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC00152 and Myeloid cell leukemia-1 (MCL-1) were targeted by miR-125b and had the same miR-125b combining site. The miR-125b level was negatively correlated with the expression of LINC00152, while MCL-1 was positively related to the LINC00152 level. MiR-125b could affect LINC00152 levels as evaluated by qRT-PCR. Finally, we affirmed that LINC00152 mediated cell proliferation by affecting MCL-1 expression and MCL-1-mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ceRNA) of miR-125b. In summary, based on ceRNA theory, the combined research on miR-125b and MCL-1, and taking LINC00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer.Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA expression was found to relate to the development and pathogenesis of multiple cancers. LncRNA LINC00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC00152 and Myeloid cell leukemia-1 (MCL-1) were targeted by miR-125b and had the same miR-125b combining site. The miR-125b level was negatively correlated with the expression of LINC00152, while MCL-1 was positively related to the LINC00152 level. MiR-125b could affect LINC00152 levels as evaluated by qRT-PCR. Finally, we affirmed that LINC00152 mediated cell proliferation by affecting MCL-1 expression and MCL-1-mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ceRNA) of miR-125b. In summary, based on ceRNA theory, the combined research on miR-125b and MCL-1, and taking LINC00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer. Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA expression was found to relate to the development and pathogenesis of multiple cancers. LncRNA LINC00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC00152 and Myeloid cell leukemia‐1 (MCL‐1) were targeted by miR‐125b and had the same miR‐125b combining site. The miR‐125b level was negatively correlated with the expression of LINC00152, while MCL‐1 was positively related to the LINC00152 level. MiR‐125b could affect LINC00152 levels as evaluated by qRT‐PCR. Finally, we affirmed that LINC00152 mediated cell proliferation by affecting MCL‐1 expression and MCL‐1‐mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ceRNA) of miR‐125b. In summary, based on ceRNA theory, the combined research on miR‐125b and MCL‐1, and taking LINC00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer. LINC00152 is upregulated in ovarian cancer tissues and cell lines. LINC00152 is a target of miR‐125b and modulates its target MCL‐1. LINC00152/miR‐125b/MCL‐1 axis modulated mitochondrial apoptosis pathway on cell apoptosis in ovarian cancer cells. |
| Author | Wu, Xiaoying Xia, Bing Li, Qiaoyan Fang, Xiaolin Zhao, Yan Chen, Puxiang |
| AuthorAffiliation | 2 Hunan Cancer Hospital Changsha China 3 Department of Gynecology and Obstetrics The Maternal and Child Health Hospital of Hunan Province Changsha China 6 Department of Pathology School of Basic Medical Science Central South University Changsha China 4 Department of Gynecology and Obstetrics The Third Xiangya Hospital of Central South University Changsha China 1 Department of Gynecology and Obstetrics The Second Xiangya Hospital of Central South University Changsha China 5 Department of Pathology Xiangya Hospital Central South University Changsha China |
| AuthorAffiliation_xml | – name: 2 Hunan Cancer Hospital Changsha China – name: 1 Department of Gynecology and Obstetrics The Second Xiangya Hospital of Central South University Changsha China – name: 6 Department of Pathology School of Basic Medical Science Central South University Changsha China – name: 3 Department of Gynecology and Obstetrics The Maternal and Child Health Hospital of Hunan Province Changsha China – name: 5 Department of Pathology Xiangya Hospital Central South University Changsha China – name: 4 Department of Gynecology and Obstetrics The Third Xiangya Hospital of Central South University Changsha China |
| Author_xml | – sequence: 1 givenname: Puxiang orcidid: 0000-0003-2600-0490 surname: Chen fullname: Chen, Puxiang email: 503157@csu.edu.cn organization: The Second Xiangya Hospital of Central South University – sequence: 2 givenname: Xiaolin surname: Fang fullname: Fang, Xiaolin organization: The Second Xiangya Hospital of Central South University – sequence: 3 givenname: Bing surname: Xia fullname: Xia, Bing organization: Hunan Cancer Hospital – sequence: 4 givenname: Yan surname: Zhao fullname: Zhao, Yan organization: The Maternal and Child Health Hospital of Hunan Province – sequence: 5 givenname: Qiaoyan surname: Li fullname: Li, Qiaoyan organization: The Third Xiangya Hospital of Central South University – sequence: 6 givenname: Xiaoying surname: Wu fullname: Wu, Xiaoying organization: Central South University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30030896$$D View this record in MEDLINE/PubMed |
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| Snippet | Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA expression... Recently, an increasing number of studies have focused on the key function of long noncoding RNA s (lnc RNA s) in biological activity. Abnormal lnc RNA... Recently, an increasing number of studies have focused on the key function of long noncoding RNA s (lnc RNA s) in biological activity. Abnormal lnc RNA... Abstract Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA... |
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| SubjectTerms | Adult Aged Apoptosis Apoptosis - genetics Biological activity Cancer Biology Cell growth Cell Line, Tumor Cell Movement Cell Proliferation competitive endogenous RNA Female Gene Expression Regulation, Neoplastic Genes, Reporter Humans Immunohistochemistry LINC00152 long noncoding RNA MCL‐1 MicroRNAs - genetics Middle Aged MiR‐125b Mitochondria Mitochondria - genetics Mitochondria - metabolism mitochondrial apoptosis pathways Myeloid Cell Leukemia Sequence 1 Protein - genetics Myeloid Cell Leukemia Sequence 1 Protein - metabolism Neoplasm Grading Original Research Ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Ribonucleic acid RNA RNA Interference RNA, Long Noncoding - genetics Signal Transduction Tumor cell lines |
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| Title | Long noncoding RNA LINC00152 promotes cell proliferation through competitively binding endogenous miR‐125b with MCL‐1 by regulating mitochondrial apoptosis pathways in ovarian cancer |
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