The clinicopathological significance of miR-1307 in chemotherapy resistant epithelial ovarian cancer

Zhou, Yingying; Wang, Min; Wu, Jianlei; Jie, Zhihui; Chang, Shuang; Shuang, Ting

doi:10.1186/s13048-015-0143-5

Cited by 37 publications

(35 citation statements)

References 38 publications

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“…Among these 2 miRNAs, miR-NA-425 has been associated with tumor stage in gastric (32) and lung cancer (33), and in RCC, it has been suggested as being a potential ccRCC biomarker (34) associated with poor prognosis for chromophobe RCC (35) and decreased PFS during sunitinib treatment (17). miR-1307 plays a role in chemoresistance in ovarian cancer (36), and it has been suggested to contribute to colorectal carcinogenesis (37). Its role in RCC is less clear, since its association with this tumor has not been described before.…”

Section: Discussionmentioning

confidence: 99%

Deep sequencing reveals microRNAs predictive of antiangiogenic drug response

García-Donás¹,

Beuselinck²,

Inglada-Pérez³

et al. 2016

JCI Insight

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Section: Discussionmentioning

confidence: 99%

Deep sequencing reveals microRNAs predictive of antiangiogenic drug response

García-Donás¹,

Beuselinck²,

Inglada-Pérez³

et al. 2016

JCI Insight

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“…MiRNAs, as transcriptional repressors, regulate gene expression by directly binding the 3’ untranslated region of their target miRNAs [2, 5, 6]. Numerous studies had proved that miRNAs are involved in regulation of almost all cellular processes including proliferation and apoptosis [2, 5–7]. Recently, miRNAs have been reported to either promote carcinogenesis by inhibiting tumor suppressors or suppress tumor development by acting as down-regulate oncogenes in ovarian cancer: downregulated miRNAs (including let-7a/b/d/f, miR-31, 34abc, 92a, 99b, 125b, 127, 152, 155 and 199a), and over-expressed oncogenic miRNAs (such as miR-18a, 20a, 21, 23a/b, 29a, 92, 93, 126, 141, 199a-3p, 200b/c and 429) [2, 8–12].…”

Section: Introductionmentioning

confidence: 99%

“…Additionally, up-regulation of miR-300 can inhibit cellular apoptosis through TGF-β, resulting in chemoresistance enhancement in ovarian cancer cells [16]. Particularly, it has been reported that miRNA-1307 is over-expressed in chemoresistant ovarian cancer tissues compared to the chemosensitive counterparts, indicating that miR-1307 is associated with the chemoresistance in ovarian cancer [7]. However, up to now, the functional study of miR-1307 has been limited, and the chemoresistance mechanism of miR-1307 in ovarian cancer is still unclear.…”

Section: Introductionmentioning

confidence: 99%

MiR-1307 promotes ovarian cancer cell chemoresistance by targeting the ING5 expression

et al. 2017

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BackgroundWe aimed to investigate the function of miR-1307 in chemoresistance and to explore its chemoresistance mechanism in ovarian cancer.MethodsIC50 determination was used to test the chemoresistance profling in ovarian cancer cells. QRT-PCR or western blot was used to validate the expression level of miR-1307 and candidate gene or protein. Colony formation assay and FITC-labeled enhanced Annexin V immunofluorescence were used to compare cell proliferation and apoptosis ability, respectively. The potential target gene and its biological function of miRNA-1307 were also analyzed. Bioinformatics and Luciferase Reporter Gene Assay were conducted to validate the regulation of miRNA-1307 on the ING5 expression. Xenografts assay was used to demonstrate the inhibiting effect of miR-1307 ASO and Taxol therapy against ovarian cancer in vivo.ResultsMiR-1307 was over-expressed in chemoresistant ovarian cancer cell line A2780/Taxol, and over-expression or loss of miR-1307 promoted or inhabited chemoresistance. And we also found that the over-expression of miR-1307 promoted proliferation and inhibited apoptosis in ovarian cancer cells. Besides, we demonstrated that ING5 was a direct target of miR-1307 and miR-1307 down-regulated the ING5 expression in ovarian cancer cells. Additionally, we showed that ING5 inhibited cell proliferation, promoted cell apoptosis and inhabited chemoresistance reversely. Furthermore, the up-regulated ability of cell apoptosis and down-regulated ability of chemoresistance following the loss of miR-1307 was reversed by adding ING5 siRNA in vitro. Finally, we proved the inhibiting effect of miR-1307 ASO and Taxol therapy by increasing the ING5 expression against ovarian cancer through xenografts assay in vivo.ConclusionOur results suggested that miR-1307 could promote ovarian cancer chemoresistance by targeting the ING5 expression and miR-1307 might serve as a therapeutic target for ovarian cancer.

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“…Epithelial ovarian cancer (EOC), a major subtype accounting for ~90% cases of ovarian cancer, includes serous adenocarcinoma, endometrial adenocarcinoma and clear cell carcinoma (3). Among the gynecological cancers, EOC has the highest mortality rate, and contributes to >50% of gynecological cancer mortalities (4). At present, the primary therapeutic strategies for EOC are surgical resection of the visible disease, followed by platinum-based chemotherapy (5).…”

Section: Introductionmentioning

confidence: 99%

microRNA-494 is a potential prognostic marker and inhibits cellular proliferation, migration and invasion by targeting SIRT1 in epithelial ovarian cancer

Yang

Wang

et al. 2017

Oncology Letters

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Abstract. Ovarian cancer is one of the most common types of gynecological malignancy worldwide, and is the fourth leading cause of cancer-associated mortality among women. Despite improvements in therapeutic treatments, the prognosis for epithelial ovarian cancer (EOC) remains poor, mainly due to the rapid growth and metastasis of ovarian cancer tumors. An increasing number of studies have indicated that microRNAs (miRNAs) are involved in the carcinogenesis and progression of human cancer, suggesting that miRNAs may be used in clinical prognosis and as a therapeutic target in EOC. The aim of the present study was to investigate the expression levels of miRNA-494 in EOC tissues and cell lines. The clinical significance of miRNA-494 in patients with EOC was also evaluated. The results demonstrated that miRNA-494 was significantly downregulated in EOC tissues and cell lines. Low expression levels of miRNA-494 were associated with poor prognostic features, including International Federation of Gynecology and Obstetrics stage, tumor size and lymph node metastasis. In vitro functional studies demonstrated that overexpression of miRNA-494 inhibited proliferation, migration and invasion in EOC cells. By contrast, knockdown of miRNA-494 enhanced cell growth, migration and invasion in EOC cells. Notably, sirtuin 1 (SIRT1) was identified as a direct target of miRNA-494 in EOC. Furthermore, MTT, cell migration and invasion assays verified that EOC cell proliferation, migration and invasion were completely restored with forced miRNA-494 expression and SIRT1 restoration. Together, these findings suggest that miRNA-494 is a potential prognostic marker, and may provide novel therapeutic regimens of targeted therapy for EOC.

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The clinicopathological significance of miR-1307 in chemotherapy resistant epithelial ovarian cancer

Cited by 37 publications

References 38 publications

Deep sequencing reveals microRNAs predictive of antiangiogenic drug response

Deep sequencing reveals microRNAs predictive of antiangiogenic drug response

MiR-1307 promotes ovarian cancer cell chemoresistance by targeting the ING5 expression

microRNA-494 is a potential prognostic marker and inhibits cellular proliferation, migration and invasion by targeting SIRT1 in epithelial ovarian cancer

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