miR-509-3p Promotes Cisplatin-Induced Apoptosis in Ovarian Cancer Cells Through the Regulation of Anti-Apoptotic Genes

Chen, Wei; Du, Jingjie; Li, Xiaodi; Su, Jiancheng; Huang, Yongzhi; Ding, Nan; Zhang, Mengdie; Jiang, Siqi

doi:10.2217/pgs-2017-0115

Cited by 26 publications

(18 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MiR-509-3p has been reported to sensitize ovarian cancer cells to cisplatin treatment by targeting multiple anti-apoptosis genes including BCL2 [129,130] . Niu et al [131] compared the expression profiles of miRNAs between three pairs of platinum-resistant and platinum-sensitive ovarian tissues and found that miR-509-3p was significantly down-regulated in cisplatin-resistant ovarian cancer tissues.…”

mentioning

confidence: 99%

Resistance to cis- and carboplatin initiated by epigenetic changes in ovarian cancer patients

Schwarzenbach¹,

Gahan²

2019

CDR

View full text Add to dashboard Cite

Initially, most ovarian tumors respond to the treatment with platinum components, but frequently recurrence occurs within the following two years in advanced ovarian cancer patients. In this regard, previous studies have shown changes in the epigenetic patterns in ovarian cancer that are linked with resistance to cis-and carboplatin therapy. Thus, epigenetic changes mediated by a treatment with cis-or carboplatin could identify such patients who do or do not respond to this therapy. Therefore, an understanding of the impact of platinum on epigenetics in ovarian cancer is important in overcoming platinum resistance. In this review, we delineate epigenetic abnormalities in cis-and carboplatin-resistant ovarian tumors, such as changes in DNA methylation, histone modifications and deregulation of microRNAs, and discuss the potential of epigenetic therapies in combination with platinum.

show abstract

mentioning

confidence: 99%

Resistance to cis- and carboplatin initiated by epigenetic changes in ovarian cancer patients

Schwarzenbach¹,

Gahan²

2019

CDR

View full text Add to dashboard Cite

show abstract

“…Then in 2013, Rao et al found that miR‐106a inhibited OVC cell A2780's survival by suppressing MCL1 gene expression. Then there were miR‐29b, miR‐491‐5p, miR‐509‐3p,, and miR‐142‐5p that were subsequently reported to play proto‐oncogenic or anti‐oncogenic roles in OVC initiation and progression . The target miRNAs varies; however, the working mechanisms are similar.…”

Section: Discussionmentioning

confidence: 99%

“…Then there were miR-29b, miR-491-5p, miR-509-3p,, and miR-142-5p that were subsequently reported to play proto-oncogenic or anti-oncogenic roles in OVC initiation and progression. 10,22,29,30 The target miRNAs varies; however, the working mechanisms are similar. We reckon that a complicated network exists while cancer The difference among the groups was analyzed using one-way ANOVA.…”

Section: Discussionmentioning

confidence: 99%

miR‐153‐3p regulates progression of ovarian carcinoma in vitro and in vivo by targeting MCL1 gene

Cui

Zhang

Zhao

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

The study of either miR‐153‐3p or MCL1 gene in ovarian carcinoma (OVC) has been reported; however, the interaction between miR‐153‐3p and MCL1 gene in OVC as well as the influence of their interaction on OVC progression has not been reported yet. Herein we intended to study the effects of miR‐153‐3p/MCL1 axis in OVC. Web‐based bioinformatics algorithms including DIANA TarBase 8.0, PicTar, and TargetScan Human 7.2 were used to predict the microRNAs (miRNAs) that could target MCL1 mRNA. Patient characteristics data collection and tissue sample immunohistochemical staining were used to determine the expression level of miR‐153‐3p and MCL1. We determined to unravel the effects of the pairing‐up of miR‐153‐3p and MCL1 mRNA in OVC cell lines (OVCAR3 cell line and A2780) and xenografts (immunodeficient(immunodeficient Rag−/− mice) using several methods including real‐time quantitative reverse transcription polymerase chain reaction, westernWestern blot, colony formation assay, wound healing assay, Transwell invasion assay, flow cytometry assay, and xenograft assay. These experiments were performed to study OVC cellular activities such as cell growth and death and so forth in vitro and in vivo. Plenty of miRNAs that can target MCL1 mRNA have been identified, and we have narrowed them down to miR‐153‐3p. MCL1 gene was found overexpressed in OVC tissues and OVC cell lines at RNA and protein levels, whereas miR‐153‐3p was found under‐expressed in OVC tissues and cells. miR‐153‐3p was found to target MCL1 mRNA and interfered OVC progression. The repression of MCL1 gene expression caused by either miR‐153‐3p or small interfering RNA technique led to significantly reduced OVC cell growth and invasion in vitro. Lastly, the engraftment of transfected human OVC cells into Rag−/− mice confirmed the in vitro results. MCL1 gene acts as a cancer facilitator in OVC. In this study, we revealed the role of miR‐153‐3p on OVC progression by targeting MCL1 gene. Our work could comprehend the current understanding of OVC progression and contribute to the underlying aggression mechanism of this cancer.

show abstract

“…The normal cell nuclei were faint staining (cells were alive). The apoptotic cell nuclei were brightness ( 18 ).…”

Section: Methodsmentioning

confidence: 99%

FPOA induces apoptosis in HeLa human cervical cancer cells through a caspase‑mediated pathway

Bau

Bao

2018

Oncol Lett

View full text Add to dashboard Cite

In the present study, the triterpenoid 3-acetoxylanosta-8,24-dien-21-oic acid (FPOA) was extracted from Fomitopsis pinicola. The aim of the present was to elucidate the mechanism of action of FPOA in HeLa cervical cancer cells. Cell viability was examined using an MTT assay and the morphological detection of apoptosis was conducted using DAPI staining. The rate of apoptosis was examined via Annexin V-FITC/PI double staining and the expression levels of apoptosis-associated proteins were determined by western blot analysis. FPOA was observed to inhibit HeLa cell proliferation, with IC50 values of 25.28, 15.30 and 11.79 µg/ml at 24, 48 and 72 h, respectively. Typical apoptotic bodies were observed in the HeLa cells following treatment with FPOA, as revealed by DAPI staining. The percentage of apoptotic cells was 3.00, 3.12, 6.18 and 32.28% following treatment with FPOA at concentrations of 0, 7.5, 15 and 30 µg/ml, respectively. Western blot analysis showed that caspase-3 and −9 were cleaved more frequently after treatment with FPOA. Furthermore, the expression of Bax was increased but Bcl-2 expression was decreased after treatment with FPOA. These results suggest that FPOA can induce HeLa cell apoptosis through a caspase-mediated pathway.

show abstract

miR-509-3p Promotes Cisplatin-Induced Apoptosis in Ovarian Cancer Cells Through the Regulation of Anti-Apoptotic Genes

Abstract: Our study demonstrates that miR-509-3p could sensitize ovarian cancer cells to cisplatin treatment by targeting multiple anti-apoptosis genes including BCL2.

Cited by 26 publications

References 28 publications

Resistance to cis- and carboplatin initiated by epigenetic changes in ovarian cancer patients

Resistance to cis- and carboplatin initiated by epigenetic changes in ovarian cancer patients

miR‐153‐3p regulates progression of ovarian carcinoma in vitro and in vivo by targeting MCL1 gene

FPOA induces apoptosis in HeLa human cervical cancer cells through a caspase‑mediated pathway

Contact Info

Product

Resources

About