miR‐1915 inhibits Bcl‐2 to modulate multidrug resistance by increasing drug‐sensitivity in human colorectal carcinoma cells

Xu, Ke; Liang, Xin; Cui, Daling; Wu, Yi-Ting; Shi, Wei; Liu, Jianwen

doi:10.1002/mc.21832

Cited by 95 publications

(66 citation statements)

References 36 publications

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“…The other related studies almost focused on either 5-fluorouracil (Song et al, 2009;Boni et al, 2010;Valeri et al, 2010;Nishida et al, 2012) or oxaliplatin (Akao et al, 2011;Chai et al, 2011;Xu et al, 2012;Xu et al, 2013). Compared with the studies about one single agent, our work served the clinical practice better.…”

Section: Discussionmentioning

confidence: 92%

Serum miR-19a Predicts Resistance to FOLFOX Chemotherapy in Advanced Colorectal Cancer Cases

Chen¹,

Xiao²,

Ge³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Background: Colorectal cancer is the fourth most common cancer worldwide and the second leading cause of cancer-related death. FOLFOX is the most common regimen used in the first-line chemotherapy in advanced colorectal cancer, but only half of the patients respond to this regimen and we have almost no clue in predicting resistance in such first-line application. Methods: To explore the potential molecular biomarkers predicting the resistance of FOLFOX regimen as the first-line treatment in advanced colorectal cancer, we screened microRNAs in serum samples from drug-responsive and drug-resistant patients by microarrays. Then differential microRNA expression was further validated in an independent population by reverse transcription and quantitative realtime PCR. Results: 62 microRNAs expressing differentially with fold-change >2 were screened out by microarray analysis. Among them, 5 (miR-221, miR-222, miR-122, miR-19a, miR-144) were chosen for further validation in an independent population (N=72). Our results indicated serum miR-19a to be significantly up-regulated in resistance-phase serum (p=0.009). The ROC curve analysis showed that the sensitivity of serum miR-19a to discriminate the resistant patients from the response ones was 66.7%, and the specificity was 63.9% when the AUC was 0.679. We additionally observed serum miR-19a had a complementary value for cancer embryonic antigen (CEA). Stratified analysis further revealed that serum miR-19a predicted both intrinsic and acquired drug resistance. Conclusions: Our findings confirmed aberrant expression of serum miR-19a in FOLFOX chemotherapy resistance patients, suggesting serum miR-19a could be a potential molecular biomarker for predicting and monitoring resistance to first-line FOLFOX chemotherapy regimens in advanced colorectal cancer patients.

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Section: Discussionmentioning

confidence: 92%

Serum miR-19a Predicts Resistance to FOLFOX Chemotherapy in Advanced Colorectal Cancer Cases

Chen¹,

Xiao²,

Ge³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…For instance, miR-200c expression is down-regulated in human breast cancer cells resistant to doxorubicin MCF-7/Adriamycin. Up-regulation of miR-200c by transfecting miR-200c mimics in breast cancer cells could enhance the chemosensitivity to epirubicin [23]. MiR-93 was significantly up-regulated in cisplatin-resistant ovarian cancer cells, and down-regulating miR-93 sensitized cells to undergo apoptosis [24].…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miR-130a contributes to cisplatin resistance in ovarian cancer cells by targeting X-linked inhibitor of apoptosis (XIAP) directly

Zhang¹,

Huang²,

Zhao³

et al. 2013

ABBS

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MicroRNAs (miRNAs) are short, highly conserved small non-coding RNA molecules, which post-transcriptionally regulate genes expression and play crucial roles in diverse biological processes. Recent studies have shown that dysregulation of miRNAs might modulate the resistance of cancer cells to chemotherapeutic agents. To investigate the possible role of miR-130a in the development of cisplatin resistance in human ovarian cancer cell line A2780, we evaluated the expression of microRNA-130a (miR-130a) in the cells by the quantitative real-time reverse transcriptionpolymerase chain reaction. The results showed that miR130a was significantly down-regulated in cisplatin-resistant ovarian cancer cells. MTT assay and flow cytometry (FCM) results showed that over-expression of miR-130a regulated apoptotic activity, and thereby cisplatin chemosensitivity, in ovarian cancer cells. Furthermore, we found that miR-130a can directly target XIAP, and participate in the regulation of apoptosis. The up-regulation of miR-130a led to a significant decrease in the XIAP mRNA levels and protein levels. XIAP plays an important role in cisplatin resistance in ovarian cancer cell line A2780. Our findings suggested that miR-130a could play a role in the development of cisplatin resistance in ovarian cancer cell line A2780, at least in part by modulation of apoptosis via targeting XIAP.

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“…Bcl-2 expression is negatively correlated with p53 expression in cancer, and numerous lines of evidence suggest that p53 regulates Bcl-2 expression at the post-translational level [39][40][41][42][43][44][45]. We and others have found p53-responsive microRNAs (miR) that suppress Bcl-2, such as miR-15 [41,46], miR-16-1 [40,41,46], miR-34 [47][48][49], and miR-1915 [43,45]. p53 promotes its target miRs by binding to the promoter regions of the miRs (miR-34 [48]) and induces their expressions.…”

Section: P53 Regulation Of Apoptosis Via the Anti-apoptotic Bcl-2 Andmentioning

confidence: 99%

Cell death decision by p53 via control of the mitochondrial membrane

Dashzeveg

Yoshida

2015

Cancer Letters

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miR‐1915 inhibits Bcl‐2 to modulate multidrug resistance by increasing drug‐sensitivity in human colorectal carcinoma cells

Cited by 95 publications

References 36 publications

Serum miR-19a Predicts Resistance to FOLFOX Chemotherapy in Advanced Colorectal Cancer Cases

Serum miR-19a Predicts Resistance to FOLFOX Chemotherapy in Advanced Colorectal Cancer Cases

Downregulation of miR-130a contributes to cisplatin resistance in ovarian cancer cells by targeting X-linked inhibitor of apoptosis (XIAP) directly

Cell death decision by p53 via control of the mitochondrial membrane

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