miR-152 is involved in the proliferation and metastasis of ovarian cancer through repression of ERBB3

Li, Lian-Wei; Xiao, Hongqi; Ma, Rong; Yang, Meng; Wan, Li; Lou, Ge

doi:10.3892/ijmm.2017.3324

Cited by 15 publications

(16 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results indicated that miR-152 had a tumor suppressive role in chordoma, consistent with its role in other human cancers, including nasopharyngeal carcinoma, endometrial cancer, and ovarian cancer. [11][12][13] Information on the downstream targets of miRNAs will help us to understand the roles of miRNAs. [7][8][9][11][12][13] Several miR-152 target genes have recently been validated in human cancers.…”

Section: Discussionmentioning

confidence: 99%

“…11 Furthermore, miR-152 inhibited endometrial cancer cell proliferation and arrested the cell cycle at G2/M phase by targeting cell division cycle 25B (CDC25B). 12 A previous study by Li et al 13 showed that miR-152 participated in the proliferation and metastasis of ovarian cancer through targeting ERBB3. However, the function of miR-152 in chordoma requires further investigation.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

RETRACTED: miR-152 inhibits the proliferation and invasion of chordoma cells by targeting HOXC8

Fang

Yan

2019

J Int Med Res

View full text Add to dashboard Cite

Objective MicroRNAs (miRNAs) are non-coding RNAs that affect the expression of their target genes by binding to the 3′-untranslated region. miR-152 has been identified as a critical modulator in tumorigenesis, but its role in chordoma has not been explored. We therefore investigated the role of miR-152 in regulating chordoma cell behavior, and examined the downstream effectors of miR-152. Materials and methods We examined the expression of miR-152 in two human chordoma cell lines and in a normal human embryonic kidney cell line. We also analyzed the relationship between miR-152 and homeobox C8 ( HOXC8) by bioinformatics analysis and luciferase reporter assay. We determined the effects of miR-152 and HOXC8 expression on chordoma cell behavior. Results miR-152 expression was downregulated in chordoma compared with normal cells. Meanwhile, miR-152 overexpression inhibited chordoma cell proliferation and invasion. The oncogene HOXC8 was a direct target of miR-152, as shown by luciferase reporter and western blot assays. Conclusions HOXC8 acted as an effector for the suppressive role of miR-152 in chordoma, thereby providing a potential therapeutic target in patients with chordoma.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

RETRACTED: miR-152 inhibits the proliferation and invasion of chordoma cells by targeting HOXC8

Fang

Yan

2019

J Int Med Res

View full text Add to dashboard Cite

show abstract

“…Moreover, the role of miRNAs in the development of drug resistance in breast cancer is crucial [10][11][12]. In recent studies, miR-152 was found to be downregulated in numerous tumors, including gastric cancer, prostate cancer, and ovarian cancer, and was shown to function as a tumor suppressor [13][14][15]. More importantly, miR-152 is involved in tamoxifen resistance in estrogen receptor-positive breast cancer [16].…”

Section: Ivyspringmentioning

confidence: 99%

EPAS1 targeting by miR-152-3p in Paclitaxel-resistant Breast Cancer

Song

Zhang

et al. 2020

J. Cancer

View full text Add to dashboard Cite

Background: Paclitaxel plays a pivotal role in the chemotherapy of breast cancer, but resistance to this drug is an important obstacle in the treatment. It is reported that microRNA-152-3p (miR-152-3p) is involved in tamoxifen resistance in breast cancer, but whether it is involved in paclitaxel resistance in breast cancer remains unknown. Materials and methods: We examined the expression of miR-152-3p in breast cancer tissues and cells by qRT-PCR. After transfecting paclitaxel-resistant MCF-7/TAX cells with miR-152-3p mimics, we analyzed the function of miR-152-3p in these cells by MTT assay and flow cytometry. We screened the target gene, endothelial PAS domain-containing protein 1 (EPAS1), using bioinformatics analysis and verified it with the dual luciferase reporter gene experiment. The relationship between EPAS1 and miR-152-3p and their roles in paclitaxel resistance of breast cancer were further investigated using RNA interference and transfection techniques. Results: The expression of miR-152-3p in normal breast tissues and cells was markedly higher than that in breast cancer. Overexpression of miR-152-3p decreased the survival rate and increased the apoptosis rate and sensitivity of MCF-7/TAX cells to paclitaxel. We confirmed that EPAS1 is the target of miR-152-3p and is negatively regulated by this miRNA. Moreover, transfection with EPAS1 siRNA enhanced the susceptibility and apoptosis rate of MCF-7/TAX cells to paclitaxel. Co-transfection of miR-152-3p mimics and EPAS1 increased paclitaxel sensitivity and apoptosis induced by the drug. Conclusion: miR-152-3p inhibits the survival of MCF-7/TAX cells and promotes their apoptosis by targeting the expression of EPAS1, thereby, enhancing the sensitivity of these breast cancer cells to paclitaxel.

show abstract

“…It was also reported that miR-152 could regulate the immune response in gastric cancer through regulating B7-H1 15 . In gynecology, it was recently reported to be involved in the proliferation and metastasis of ovarian cancer through suppression of ERBB3 16 . A study showed that miR-152 expression could be induced by hypoxia, and its expression can suppress the expression of WNT1 and ERBB3 and therefore inhibit the proliferation of CC cells 17 .…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-152 Acts as a Tumor Suppressor MicroRNA by Inhibiting Krüppel-Like Factor 5 in Human Cervical Cancer

Zhang

Wang

et al. 2019

oncol res

View full text Add to dashboard Cite

Aberrant expression of microRNA-152 (miR-152) is frequently observed in human cancers including ovarian cancer, breast cancer, prostate cancer, and gastric cancer. However, its expression and functional role in cervical cancer (CC) is poorly understood. Also, the association between miR-152 and Krüppel-like factor 5 (KLF5) expression in CC remains unclear. In this study, analyzing the expression of miR-152 by quantitative real-time PCR (qRT-PCR) revealed it was sharply reduced in CC tissues and cell lines. Meanwhile, the negative correlation of miR-152 expression and KLF5 expression was observed. The dual-luciferase reporter assay validated KLF5 was a target of miR-152. In vitro functional assays revealed that miR-152 could inhibit cell proliferation and cell cycle progression through regulating the expression of KLF5. Taken together, our study suggested miR-152 functions as a tumor suppressor in CC and the miR-152/KLF5 axis may provide novel therapeutic targets for CC treatment.

show abstract

miR-152 is involved in the proliferation and metastasis of ovarian cancer through repression of ERBB3

Cited by 15 publications

References 44 publications

RETRACTED: miR-152 inhibits the proliferation and invasion of chordoma cells by targeting HOXC8

RETRACTED: miR-152 inhibits the proliferation and invasion of chordoma cells by targeting HOXC8

EPAS1 targeting by miR-152-3p in Paclitaxel-resistant Breast Cancer

MicroRNA-152 Acts as a Tumor Suppressor MicroRNA by Inhibiting Krüppel-Like Factor 5 in Human Cervical Cancer

Contact Info

Product

Resources

About