The inhibition of miR-21 promotes apoptosis and chemosensitivity in ovarian cancer

Chan, John K.; Blansit, Kevin; Kiet, T.; Sherman, Alexander E.; Wong, Gabriel; Earle, Christine; Bourguignon, Lilly Y.W.

doi:10.1016/j.ygyno.2014.01.034

Cited by 125 publications

(100 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition to the pathways in cancer and pathways related to specified cancers (such as prostate and colorectal cancer), 4 pathways including ErbB signaling, focal adhesion, apoptosis and p53 signaling were enriched, suggesting that HNF1B may contribute to drug resistance in ovarian cancer via those pathways. ErbB signaling (91), focal adhesion (92,93), apoptosis (94,95) and p53 signaling (96,97) have been reported to associate with drug resistance in ovarian cancer. For example, miR-21 regulates drug resistance via apoptosis and cellular survival pathways (94), and loss of DOK2 induces carboplatin resistance in ovarian cancer via suppression of apoptosis (98).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of HNF1 homeobox B is associated with drug resistance in ovarian cancer

Zhang²,

Gao

et al. 2014

Oncology Reports

View full text Add to dashboard Cite

Abstract. The expression of HNF1 homeobox B (HNF1B) is associated with cancer risk in several tumors, including ovarian cancer, and its decreased expression play roles in cancer development. However, the study of HNF1B and cancer is limited, and its association with drug resistance in cancer has never been reported. On the basis of array data retrieved from Oncomine and Gene Expression Omnibus (GEO) online database, we found that the mRNA expression of HNF1B in 586 ovarian serous cystadenocarcinomas and in platinum-resistant A2780 epithelial ovarian cancer cells was significantly decreased, indicating a potential role of HNF1B in drug resistance in ovarian cancer. Based on this finding, comprehensive bioinformatics analyses, including protein/ gene interaction, protein-small molecule/chemical interaction, biological process annotation, gene co-occurrence and pathway enrichment analysis and microRNA-mRNA interaction, were performed to illustrate the association of HNF1B with drug resistance in ovarian cancer. We found that among the proteins/ genes, small molecules/chemicals and microRNAs which directly interacted with HNF1B, the majority was associated with drug resistance in cancer, particularly in ovarian cancer. Biological process annotation revealed that HNF1B closely related to 24 biological processes which were all notably associated with ovarian cancer and drug resistance. These results indicated that the downregulation of HNF1B may contribute to drug resistance in ovarian cancer, via its direct interactions with these drug resistance-related proteins/genes, small molecules/chemicals and microRNAs, and via its regulations on the drug resistance-related biological processes. Pathway enrichment analysis of 36 genes which co-occurred with HNF1B, ovarian cancer and drug resistance indicated that the HNF1B may perform its drug resistance-related functions through 4 pathways including ErbB signaling, focal adhesion, apoptosis and p53 signaling. Collectively, in this study, we illustrated for the first time that HNF1B may contribute to drug resistance in ovarian cancer, potentially through the 4 pathways. The present study may pave the way for further investigation of the drug resistance-related functions of HNF1B in ovarian cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

Downregulation of HNF1 homeobox B is associated with drug resistance in ovarian cancer

Zhang²,

Gao

et al. 2014

Oncology Reports

View full text Add to dashboard Cite

show abstract

“…99,100 In addition, exploration of natural compounds may help identify novel drugs to regulate the miR-21/PDCD4 axis in cancer cells. One example is the use of Berberine to inhibit miR-21 expression and function in ovarian cancer leading to enhancement of its target PDCD4.…”

Section: Targeted Therapeutic Strategies For Mir-21 and Pdcd4 In Gbmmentioning

confidence: 99%

Targeting strategies on miRNA-21 and PDCD4 for glioblastoma

Wang

Tang

et al. 2015

Archives of Biochemistry and Biophysics

View full text Add to dashboard Cite

“…Additionally, miR-29b and its signaling mechanism involved in patients with ovarian cancer [8]. The inhibition of miR-21 promotes apoptosis and, thus causes drug sensitivity in ovarian cancer [9]. The miR-197 contributes to paclitaxel resistance in ovarian cancer cells [10].…”

Section: Introductionmentioning

confidence: 99%

Down‐regulated expression of miR‐134 contributes to paclitaxel resistance in human ovarian cancer cells

et al. 2015

View full text Add to dashboard Cite

a b s t r a c tMiR-134 has been reported to have a role in the development and progression of various cancers. In this study, we found that miR-134 expression was significantly decreased in chemo-resistant serous epithelial ovarian cancer (EOC) patients. Over-expression of miR-134 enhanced the sensitivity of SKOV3-TR30 cells to paclitaxel, and increased paclitaxel-induced apoptosis. Further, Pak2 was identified as a direct target of miR-134, and Pak2-specific siRNA increased cell inhibition rate and promoted paclitaxal-induced apoptosis. By regulating Pak2 expression, miR-134 could mediate Bad phosphorylation at Ser112 and Ser136, which affected cell survival and apoptosis. In conclusion, our findings indicate that repression of miR-134 and consequent up-regulation of Pak2 might contribute to paclitaxel resistance.

show abstract

The inhibition of miR-21 promotes apoptosis and chemosensitivity in ovarian cancer

Cited by 125 publications

References 37 publications

Downregulation of HNF1 homeobox B is associated with drug resistance in ovarian cancer

Downregulation of HNF1 homeobox B is associated with drug resistance in ovarian cancer

Targeting strategies on miRNA-21 and PDCD4 for glioblastoma

Down‐regulated expression of miR‐134 contributes to paclitaxel resistance in human ovarian cancer cells

Contact Info

Product

Resources

About