miR-214 promotes radioresistance in human ovarian cancer cells by targeting PETN

Zhang, Qin; Zhang, Shuxiang

doi:10.1042/bsr20170327

Cited by 33 publications

(28 citation statements)

References 38 publications

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“…Several studies have demonstrated that miRNAs are involved in regulating various biological processes, including cell proliferation ( 11 ), migration ( 10 ), invasion ( 10 , 12 ) and drug resistance ( 13 ). miR-214, one member of the miR-214 family, has been revealed to be aberrantly expressed in several human cancer types, including breast cancer ( 14 ), hepatocellular carcinoma ( 15 ), lung cancer ( 13 ), esophageal squamous cell cancer ( 16 ) and ovarian cancer ( 17 ). The dysregulation of miR-214 predicts a poor prognosis in the aforementioned cancers ( 13 – 17 ).…”

Section: Introductionmentioning

confidence: 99%

microRNA‑214 suppresses the growth of cervical cancer cells by targeting EZH2

Yang

Liu

et al. 2018

Oncol Lett

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A number of studies have revealed the significance of microRNAs (miRs) in tumorigenesis. Cervical cancer (CC) is one of the most malignant cancer types and is associated with a poor overall survival rate. A previous study demonstrated a critical role of miR-214 in the development of multiple cancer types, but its role in CC remains elusive. In the current study, miR-214 was observed to be downregulated in CC tissues compared with the adjacent non-cancerous tissue. Overexpression of miR-214 reduced the proliferation of CC cells, whereas inhibiting its expression resulted in enhanced proliferation. Furthermore, Enhancer of zeste homolog 2 (EZH2) was demonstrated to be a direct target of miR-214 in CC. An MTT assay demonstrated that upregulating miR-214 expression or knocking down the expression of EZH2 impaired the proliferation of a CC cell line. Low expression of miR-214 was positively associated with tumor differentiation (P=0.037) and tumor stage (P=0.012). Notably, low expression of miR-214 predicted poor prognosis of patients with CC. Consequently, the results of the current study demonstrated that miR-214 functions as a tumor suppressor in CC and may be regarded as a potential therapeutic target in CC.

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Section: Introductionmentioning

confidence: 99%

microRNA‑214 suppresses the growth of cervical cancer cells by targeting EZH2

Yang

Liu

et al. 2018

Oncol Lett

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“…Yang et al [18] and Li et al [19] also found miR-214 acts as a tumor suppressor in liver cancer proliferation and cell cycle. There also some different view, many researchers showed miR-214 promoted tumor pathogenesis, such as in gastric cancer cell [20, 21], ovarian cancer cells [22]. However, the roles of miR-214-5p on HCC invasion remain unknown.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-214-5p Inhibits the Invasion and Migration of Hepatocellular Carcinoma Cells by Targeting Wiskott-Aldrich Syndrome Like

Wang

Ren³

2018

Cell Physiol Biochem

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Background/Aims: This study aims to explore the effects of microRNA-214-5p (miR-214-5p) on the invasion and migration of Hepatocellular Carcinoma cells (HCC). Methods: Hepatocellular Carcinoma tissues and adjacent normal tissues from 44 hepatocellular carcinoma patients were prepared for this study. The HepG2 and BEL-7402 cells were transfected with miR-214-5p mimic and inhibitor. qRT-PCR was performed to detect the expressions of miR-214-5p. Transwell assays were used to detect the invasion and migration assays in HepG2 and BEL-7402 cells. A dual-luciferase reporter assay was conducted to examine the effect of miR-214-5p on Wiskott-Aldrich Syndrome Like (WASL/ N-WASP). Western blot and qRT-PCR were used to measure the expressions of the E-cadherin, N-cadherin and Vimentin proteins. Transwell chamber assays were performed to detect cell invasion and migration. Results: Compared with normal tissues, HCC tissues demonstrated significantly lower expression of miR-214-5p. Overexpression of miR-214-5p significantly inhibited the migration and invasion of HCC cells and inhibition of miR-214-5p promoted the migration and invasion. Additionally, miR-214-5p suppressed the epithelial-mesenchymal transition (EMT). Further study showed WASL was a putative target gene of miR-214-5p. Up-regulating the expression of WASL could reverse the inhibition effect of miR-214-5p on invasion and migration. Conclusion: Our data suggested that miR-214-5p inhibited the invasion and migration of HepG2 and BEL-7402 by targeting WASL in Hepatocellular carcinoma.

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“…MiR-668 overexpression decreases the IκBα level, increases NF-κB, and then enhances radioresistance in BC cell lines [182]. Besides, in OC, IR upregulates the expression of miR-214 in vitro and in vivo, which depresses PETN and consequently activates the PI3K/Akt pathway, resulting in radioresistance [183]. Taken together, these studies provide fresh insight into the contribution of miRNAs in multiple cancers radiation resistance, and it is essential to identify more miRNAs that can be potential therapeutic targets for radioresistant cancer patients.…”

Section: Other Cancersmentioning

confidence: 99%

“…Radiotherapy is an essential approach for locally advanced CC. However, around 30% of radiotherapy- Lung cancer miR -198 Inhibiting HGF/c-MET pathway [170] miR-99a Binding to mTOR [171] miR-558 Associating with AATK [172] miR-148b Modulating MutL homologue 1 [173] miR-335 Reducing the expression of PARP-1, downregulating NF-κB [ 174] miR-1246 Inhibiting DR5 [175] miR-21 Upregulating HIF-1α [176] miR-208a Targeting p21 with a corresponding activation of the Akt/mTOR pathway [177] Oral cancer stem cells miR-218 Activating miR-218/Bmi1 axis [178] Hepatocellular carcinoma miR-92b Reducing p57kip2 expression [179] Breast cancer miR-142-3p Attenuating CSCs characteristics and inhibiting β-catenin expression [180] miR-22 Negatively modulating Sirt1 [181] miR-668 Forming miR-668/ IκBα/NF-κB axis [182] Ovarian cancer miR-214 Depressing PETN and consequently activating PI3K/Akt pathway [183] treated patients have been found occurring recurrence or even metastasis, partially resulting from radioresistance. It has been reported that miRNAs participate in either radiation responsiveness or radioresistance.…”

Section: CCmentioning

confidence: 99%

Role of non-coding RNAs and RNA modifiers in cancer therapy resistance

et al. 2020

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As the standard treatments for cancer, chemotherapy and radiotherapy have been widely applied to clinical practice worldwide. However, the resistance to cancer therapies is a major challenge in clinics and scientific research, resulting in tumor recurrence and metastasis. The mechanisms of therapy resistance are complicated and result from multiple factors. Among them, non-coding RNAs (ncRNAs), along with their modifiers, have been investigated to play key roles in regulating tumor development and mediating therapy resistance within various cancers, such as hepatocellular carcinoma, breast cancer, lung cancer, gastric cancer, etc. In this review, we attempt to elucidate the mechanisms underlying ncRNA/modifier-modulated resistance to chemotherapy and radiotherapy, providing some therapeutic potential points for future cancer treatment.

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miR-214 promotes radioresistance in human ovarian cancer cells by targeting PETN

Cited by 33 publications

References 38 publications

microRNA‑214 suppresses the growth of cervical cancer cells by targeting EZH2

microRNA‑214 suppresses the growth of cervical cancer cells by targeting EZH2

MicroRNA-214-5p Inhibits the Invasion and Migration of Hepatocellular Carcinoma Cells by Targeting Wiskott-Aldrich Syndrome Like

Role of non-coding RNAs and RNA modifiers in cancer therapy resistance

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