lncRNAs are novel biomarkers for differentiating between cisplatin‑resistant and cisplatin‑sensitive ovarian cancer

Li, Qing; Zhang, Juan; Zhou, Juan; Yang, Binglie; Li, Pingping; Cao, Lei; Lei, Jing; Liu, Hua

doi:10.3892/ol.2018.8433

Cited by 11 publications

(9 citation statements)

References 46 publications

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“…Cisplatinum, a well-known chemotherapeutic drug, is widely used for treatment of HCC [15]. Accumulating evidence indicates that LncRNAs are involved in the process of cisplatinum-induced apoptosis of cancer cells and are novel biomarkers for differentiating between cisplatin-resistant and cisplatin-sensitive cancers [16, 19]. In the present study, we analyzed the LncRNA differential expressions in cisplatinum-treated hepatocellular carcinoma QGY7703 cells by RNA-seq (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…LncRNA MEG3 suppresses glioma cell proliferation, migration, and invasion by acting as a competing endogenous RNA of miR-19a [18]. Moreover, LncRNAs are reported to be novel biomarkers for differentiating between cisplatin-resistant and cisplatin-sensitive ovarian cancer [19]. For example, knockdown of LncRNA HOTAIR sensitizes HCC cell to cisplatin by suppressing the STAT3/ABCB1 signaling pathway [20].…”

Section: Introductionmentioning

confidence: 99%

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RETRACTED ARTICLE: Long non-coding RNA TPTEP1 inhibits hepatocellular carcinoma progression by suppressing STAT3 phosphorylation

Ding

Liu

Zou

et al. 2019

J Exp Clin Cancer Res

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Background Hepatocellular carcinoma (HCC) is still the most common cause of tumor-related death worldwide and accumulating studies report that long non-coding RNAs (LncRNAs) are closely related with HCC development, metastasis and prognosis. Cisplatinum, a well-known chemotherapeutic drug, has been widely used for treatment of numerous human cancers including HCC. This study aimed to investigate the differential expressions of LncRNAs in HCC cells treated with cisplatinum and its underlying mechanism. Methods The differential expressions of LncRNAs in HCC cells treated with cisplatinum were determined by RNA-seq. The roles of TPTEP1 in HCC development by applying gene function gain and loss analysis in MHCC97H and QYG-7703 cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR), cell proliferation, colony formation, cell invasion and flow cytometry assays. The underlying mechanism of TPTEP1 sensitizing hepatocellular carcinoma cells to cisplatinum was examined by RNA-pull down, western blotting, subcellular fractionation, RNA immunoprecipitation and dual luciferase reporter assays. The effect of TPTEP1 on tumorigenesis in vivo was performed with a subcutaneous xenograft mouse model of HCC. In addition, TPTEP1 expression was detected in clinical tumor tissue samples by qRT-PCR. Results LncRNA TPTEP1 was highly expressed in cisplatinum-treated HCC cells, which sensitizes hepatocellular carcinoma cell to cisplatinum-induced apoptosis. TPTEP1 overexpression inhibited, while TPTEP1 knockdown promoted HCC cell proliferation, tumorigenicity and invasion. Furthermore, TPTEP1 exerted its tumor suppressing activities by interacting with signal transducer and activator of transcription 3 (STAT3) to inhibit its phosphorylation, homodimerization, nuclear translocation and down-stream genes transcription. Moreover, TPTEP1 overexpression obviously inhibits tumor masses in vivo in a subcutaneous xenograft mouse model of HCC and TPTEP1 is frequently downregulated in HCC tissues, compared to its corresponding pre-tumor tissues. Conclusion LncRNA TPTEP1 inhibits hepatocellular carcinoma cells progression by affecting IL-6/STAT3 signaling. Taken together, our findings suggest a tumor suppressing role of TPTEP1 in HCC progression and provide a novel understanding of TPTEP1 during the chemotherapy for HCC. Electronic supplementary material The online version of this article (10.1186/s13046-019-1193-0) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Long non-coding RNA TPTEP1 inhibits hepatocellular carcinoma progression by suppressing STAT3 phosphorylation

Ding

Liu

Zou

et al. 2019

J Exp Clin Cancer Res

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“…However, cisplatin are still the current first-line drugs for ovarian cancer and other carcinomas for its effect on inducing DNA double-strand breaks (DSBs) and apoptosis of cancer cells ( Mensah et al, 2019 ). Although chemotherapy is widely used for treating metastatic OC for the encouragingly efficiency, drug resistance remains to be a great challenge for its clinical use ( Boyd and Muggia, 2018 ; Li et al, 2018 ; Sang et al, 2018 ; Jiang et al, 2019 ; Qu et al, 2019 ). In recent years, studies indicating that lncRNAs were associated with drug sensitivity of tumor cells have been increasingly concerned.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: NEAT1 Overexpression Indicates a Poor Prognosis and Induces Chemotherapy Resistance via the miR-491-5p/SOX3 Signaling Pathway in Ovarian Cancer

2021

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BackgroundAccumulated studies have reported that dysregulated long non-coding RNAs (lncRNAs) are crucial in ovarian cancer (OC) initiation and development. However, detailed biological functions of lncRNA NEAT1 during the progression of OC remains to be uncovered.PurposeOur aim was to identify the role of NEAT1 in cisplatin resistance of ovarian cancer and the underlying mechanisms.MethodsThe expression patterns of NEAT1 in OC cell lines and tissue samples were identified by qRT-PCR. The cisplatin (DDP) sensitivity of OC cells was detected by MTT and CCK8 assay, while OC cell apoptosis and cell cycle were detected using flow cytometer assays. In addition, effects of NEAT1 on tumor growth were determined by xenograft tumor model. Luciferase reporter assay was conducted to prove the regulatory relation of miR-491-5p, NEAT1, and SOX3. Importantly, the expression of NEAT1 in exosomes from cisplatin-resistant patients was also determined by using qRT-PCR.ResultsIn this study, upregulated NEAT1 was detected in OC cell lines and tissues. Meanwhile, NEAT1 was also increased in cisplatin-resistant OC cell lines and tissues. Upregulation of NEAT1 inhibited cisplatin-induced OC cell apoptosis and promoted cell proliferation, while knockdown of NEAT1 played the opposite role. These effects were also observed in vivo. Furthermore, direct interaction was observed between NEAT1 and miR-491-5p. NEAT1 led to the upregulation of miR-491-5p-targeted SOX3 mRNA. Importantly, this study also showed upregulated NEAT1 expression in serum exosomes derived from cisplatin-resistant patients.ConclusionNEAT1 is vital in the chemoresistance of ovarian cancer through regulating miR-491-5p/SOX3 pathway, showing that NEAT1 might be a potential target for OC resistance treatment.

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“…LncRNAs have emerged as novel biomarkers to distinguish between cisplatin-resistant and cisplatin-sensitive OC. 19 Some lncRNAs have been identified as being involved in the regulation of OC cisplatin resistance. LncRNA UCA1 was found to be up-regulated in tumor tissues of OC cisplatin-resistant patients.…”

Section: Discussionmentioning

confidence: 99%

LINC00184 Promotes Ovarian Cancer Cells Proliferation and Cisplatin Resistance by Elevating CNTN1 Expression via Sponging miR-1305

Han¹,

You²,

Liu³

et al. 2021

OTT

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Objective: Cisplatin resistance is one of the main reasons for treatment failure in ovarian cancer (OC). Here, the effects of LINC00184 on cisplatin-resistant OC were studied. Patients and Methods: LINC00184, miR-1305 and CNTN1 expression in tissues from 70 OC patients was determined by qRT-PCR, in situ hybridization and Western blot. OC cell lines and OC cisplatin-resistant cell lines were cultured. Cells were transfected using Lipofectamine 2000 and treated with 100 nM cisplatin. Cell proliferation and apoptosis were researched by the CCK-8 assay and flow cytometry. A dual-luciferase reporter gene assay and RNA pull-down were performed to explore the relationship between two genes. LINC00184, miR-1305 and CNTN1 expression in cells was detected by qRT-PCR and Western blot. An in vivo experiment was conducted using nude mice. Ki67 and CNTN1 expression and apoptosis of xenograft tumors were investigated using immunohistochemistry and a TUNEL assay. Results: LINC00184 was up-regulated in OC clinical tissues and OC cells, especially in cisplatin-resistant OC patients and cells (p<0.01 or p<0.0001). LINC00184 overexpression significantly enhanced OC cell proliferation and cisplatin resistance, and inhibited OC cell apoptosis (p<0.05 or p<0.01). LINC00184 elevated CNTN1 expression via sponging miR-1305. LINC00184 overexpression markedly exacerbated the malignant phenotype of OC cells and cisplatin-resistant OC cells via the miR-1305/CNTN1 axis (p<0.01). Silencing of LINC00184 significantly suppressed OC cell growth and cisplatin resistance in vivo (p<0.01). LINC00184 silencing inhibited Ki67 and CNTN1 expression and promoted apoptosis of xenograft tumors. CNTN1 overexpression promoted proliferation and cisplatin resistance, and reduced apoptosis of OC cells (p<0.05 or p<0.01). Conclusion: LINC00184 promoted OC cell proliferation and cisplatin resistance by elevating CNTN1 expression via sponging miR-1305.

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lncRNAs are novel biomarkers for differentiating between cisplatin‑resistant and cisplatin‑sensitive ovarian cancer

Cited by 11 publications

References 46 publications

RETRACTED ARTICLE: Long non-coding RNA TPTEP1 inhibits hepatocellular carcinoma progression by suppressing STAT3 phosphorylation

RETRACTED ARTICLE: Long non-coding RNA TPTEP1 inhibits hepatocellular carcinoma progression by suppressing STAT3 phosphorylation

RETRACTED: NEAT1 Overexpression Indicates a Poor Prognosis and Induces Chemotherapy Resistance via the miR-491-5p/SOX3 Signaling Pathway in Ovarian Cancer

LINC00184 Promotes Ovarian Cancer Cells Proliferation and Cisplatin Resistance by Elevating CNTN1 Expression via Sponging miR-1305

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