miR‑200b and miR‑200c co‑contribute to the cisplatin sensitivity of ovarian cancer cells by targeting DNA methyltransferases

Liu, Jue; Zhang, Xiaobo; Huang, Yuliang; Zhang, Qunfeng; Zhou, Jiayi; Zhang, Xiaodi; Wang, Xiaoxu

doi:10.3892/ol.2018.9745

Cited by 32 publications

(37 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, the higher expression of miR-200c was exclusively associated with carcinoma at the advanced stages [128]. A study carried out by Liu and colleagues claimed that enhancing the expression of miR-200b and miR-200c could lead to apoptosis in EOC [129]. Results from this study indicated that miR-200b and miR-200c control the downregulation of DNA methyltransferase (DNMTs) and increase chemotherapeutic sensitivity in ovarian cancer cells leading to better drug efficacy and tumor suppression.…”

Section: Indirect Cellular Processes That Affect Apoptosis Inductionmentioning

confidence: 99%

Therapeutic Inducers of Apoptosis in Ovarian Cancer

Binju

Amaya-Padilla

Wan

et al. 2019

Cancers

View full text Add to dashboard Cite

Ovarian cancers remain one of the most common causes of gynecologic cancer-related death in women worldwide. The standard treatment comprises platinum-based chemotherapy, and most tumors develop resistance to therapeutic drugs. One mechanism of developing drug resistance is alterations of molecules involved in apoptosis, ultimately assisting in the cells’ capability to evade death. Thus, there is a need to focus on identifying potential drugs that restore apoptosis in cancer cells. Here, we discuss the major inducers of apoptosis mediated through various mechanisms and their usefulness as potential future treatment options for ovarian cancer. Broadly, they can target the apoptotic pathways directly or affect apoptosis indirectly through major cancer-pathways in cells. The direct apoptotic targets include the Bcl-2 family of proteins and the inhibitor of apoptotic proteins (IAPs). However, indirect targets include processes related to homologous recombination DNA repair, micro-RNA, and p53 mutation. Besides, apoptosis inducers may also disturb major pathways converging into apoptotic signals including janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3), wingless-related integration site (Wnt)/β-Catenin, mesenchymal-epithelial transition factor (MET)/hepatocyte growth factor (HGF), mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK), and phosphatidylinositol 3-kinase (PI3K)/v-AKT murine thymoma viral oncogene homologue (AKT)/mammalian target of rapamycin (mTOR) pathways. Several drugs in our review are undergoing clinical trials, for example, birinapant, DEBIO-1143, Alisertib, and other small molecules are in preclinical investigations showing promising results in combination with chemotherapy. Molecules that exhibit better efficacy in the treatment of chemo-resistant cancer cells are of interest but require more extensive preclinical and clinical evaluation.

show abstract

Section: Indirect Cellular Processes That Affect Apoptosis Inductionmentioning

confidence: 99%

Therapeutic Inducers of Apoptosis in Ovarian Cancer

Binju

Amaya-Padilla

Wan

et al. 2019

Cancers

View full text Add to dashboard Cite

show abstract

“…MicroRNAs (miRNAs/miRs) are a group of these key molecules that have been investigated in various types of cancer (9,10). These small RNAs have no capacity of protein coding, but exert regulatory roles in gene expression at the post-transcriptional level (11). In addition, miRNAs are involved in the regulation of various cell processes, such as cell proliferation, migration, invasion, differentiation, cell cycle and apoptosis (12,13).…”

Section: Introductionmentioning

confidence: 99%

Upregulated miR‑665 expression independently predicts poor prognosis of lung cancer and facilitates tumor cell proliferation, migration and invasion

Xia

Zhu

et al. 2020

Oncol Lett

View full text Add to dashboard Cite

Non-small cell lung cancer (NSCLC) is one of the leading causes of global cancer-associated mortality. Aberrant microRNAs (miRs) have been reported to be involved in the pathogenesis of various cancer types. The present study aimed to investigate the expression profile and prognostic value of miR-665 in patients with NSCLC, and to analyze its functional role in tumor progression using NSCLC cells. Reverse transcription-quantitative PCR was used to estimate the expression levels of miR-665. Kaplan-Meier survival curves and Cox regression analysis were performed to evaluate the prognostic value of miR-665. The effects of miR-665 on NSCLC cell proliferation, migration and invasion were examined by cell transfection, and the target gene of miR-665 was explored. miR-665 expression was elevated in the tissue and cell samples of NSCLC. This increased miR-665 expression was associated with lymph node metastasis and TNM stage. An independent association between miR-665 and overall survival was identified in patients with NSCLC. When regulating the expression levels of miR-665 in vitro, NSCLC cell proliferation, migration and invasion were enhanced by overexpression of miR-665, but were inhibited by knockdown of miR-665. The luciferase activity results indicated that the protein tyrosine phosphatase receptor type B (PTPRB) was a direct target of miR-665 in NSCLC cells. The present study provided evidence for the clinical significance of a decreased expression of miR-665 in the prognosis of NSCLC. Upregulation of miR-665 contributed to tumor cell proliferation, migration and invasion by targeting PTPRB, suggesting the potential of miR-665 as a candidate therapeutic target for NSCLC treatment.

show abstract

“…DNMT3A was reported as the direct target of cisplatin-sensitizing miR-200b and miR-200c in A2780/CDDP cells (J. Liu et al, 2019); however, our study first confirmed DNMT3A as a promoter of cisplatin resistance with cell models. And we first identified that DNMT3A antagonized the cisplatin-sensitizing effect of miR-143 in ovarian cancer cells.…”

Section: Discussionmentioning

confidence: 42%

The negative feedback between miR‐143 and DNMT3A regulates cisplatin resistance in ovarian cancer

Han

Liú

Zhou

et al. 2020

Cell Biology International

View full text Add to dashboard Cite

Emerging evidence suggests that miR‐143 plays an important role in the regulation of tumor sensitivity to chemotherapeutic agents. The study explores the underlying mechanism of miR‐143 in reversing cisplatin resistance in ovarian cancer. The cisplatin‐resistant ovarian cancer cell line A2780/CDDP was induced and established via treating A2780 cells by gradually increasing cisplatin concentrations. The IC50 values of A2780/CDDP and A2780 to cisplatin were 218.10 ± 1.12 and 21.99 ± 1.12 μM, respectively. Quantitative real‐time polymerase chain reaction (qRT‐PCR) results showed that miR‐143 was significantly decreased in A2780/CDDP cells compared with A2780 cells. miR‐143 overexpression decreased cisplatin resistance in A2780/CDDP, and miR‐143 inhibition decreased A2780 sensitivity to cisplatin. Results of qRT‐PCR, Western blot analysis, and luciferase reporter assay indicated that the direct target of miR‐143 was DNMT3A, which, in turn, was upregulated in A2780/CDDP. DNMT3A overexpression antagonized the sensitizing effect of miR‐143 on A2780/CDDP to cisplatin. Knocking down of DNMT3A reduced cisplatin resistance in A2780/CDDP, while overexpression of DNMT3A increased cisplatin resistance in A2780. Methylation‐specific polymerase chain reaction results showed that the methylation level in the promoter region of the miR‐143 precursor gene was higher in A2780/CDDP cells than in A2780 cells. DNMT3A mediated the hypermethylation of the miR‐143 precursor gene, resulting in miR‐143 downregulation in A2780/CDDP. miR‐143 inhibited cell growth of A2780/CDDP cell in nude mice. Our findings indicated the negative feedback between miR‐143 and DNMT3A as a crucial epigenetic modifier of cisplatin resistance in ovarian cancer.

show abstract

miR‑200b and miR‑200c co‑contribute to the cisplatin sensitivity of ovarian cancer cells by targeting DNA methyltransferases

Cited by 32 publications

References 39 publications

Therapeutic Inducers of Apoptosis in Ovarian Cancer

Therapeutic Inducers of Apoptosis in Ovarian Cancer

Upregulated miR‑665 expression independently predicts poor prognosis of lung cancer and facilitates tumor cell proliferation, migration and invasion

The negative feedback between miR‐143 and DNMT3A regulates cisplatin resistance in ovarian cancer

Contact Info

Product

Resources

About