LncRNA CAR10 Upregulates PDPK1 to Promote Cervical Cancer Development by Sponging miR-125b-5p

Hu, Tingting; Zhang, Qian; Gao, Lingxue

doi:10.1155/2020/4351671

Cited by 25 publications

(26 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…25 A recent study has displayed that the expression of CAR10 in CC tissues and cells is dramatically increased, whereas up-regulation of CAR10 is closely correlated with lymph node metastasis. 11 In another study, OIP5-AS1 expression is markedly upregulated in CC cells, which is significantly associated with lymph node metastasis and tumor stage. 9 Similarly, we found that MIR4435-2HG expression was dramatically increased in CC tissues and cells.…”

Section: Discussionmentioning

confidence: 93%

“…10 LncRNA CAR10 expression is significantly up-regulated in CC tissues, whereas overexpression of CAR10 can promote the proliferation of CC cells. 11 Additionally, the emerging evidences have displayed that lncRNA MIR4435-2HG is correlated with the occurrence and progression of many cancers. [12][13][14][15] A previous study has showed that overexpression of lncRNA MIR4435-2HG increases the cell viability and migration in colon adenocarcinoma (COAD) cells, which eventually promotes the development of colorectal cancer (CRC) in mice.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

<p>Knockdown of MIR4435-2HG Suppresses the Proliferation, Migration and Invasion of Cervical Cancer Cells via Regulating the miR-128-3p/MSI2 Axis in vitro</p>

Wang

Liu

Jiao

et al. 2020

CMAR

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) play major roles in the development of several cancers, including cervical cancer (CC). The purpose of the present study is to explore the regulatory mechanism of MIR4435-2HG on CC in vitro. Patients and Methods: Fifty-nine pairs of CC tissues and adjacent normal tissues were collected from 59 patients by resection. The expression of lncRNA MIR4435-2HG, microRNA (miR)-128-3p and Musashi 2 (MSI2) in CC tissues and cells was detected by quantitative reverse-transcription PCR (qRT-PCR). The viability of CC cells was detected by 3-(4, 5-Dimethyl-2-Thiazolyl)-2, 5-Diphenyl-2-H-Tetrazolium Bromide (MTT) assay. The ability of migration and invasion in CC cells was measured by wound healing assay and transwell invasion assay, respectively. Starbase software and Targetscan software were utilized to predict the relationship between miR-128 and MIR4435-2HG/MSI2, respectively. The dual-luciferase reporter assay was used to confirm these interactions. Results: LncRNA MIR4435-2HG expression was significantly up-regulated in CC tissues (P < 0.001) and cells (P < 0.01). Knockdown of MIR4435-2HG inhibited the proliferation, migration and invasion of CC cells (P < 0.01). MiR-128-3p was a target of MIR4435-2HG and was negatively modulated by MIR4435-2HG (P < 0.0001, r = −0.6331). Up-regulation of miR-128-3p suppressed the proliferation, migration and invasion of CC cells (P < 0.01). In addition, MSI2 was the target gene of miR-128-3p and negatively regulated by miR-128-3p (P < 0.0001, r = −0.4775). Both down-regulation of miR-128-3p and up-regulation of MSI2 reversed the inhibitory effects of MIR4435-2HG knockdown on the proliferation, migration and invasion of CC cells (P < 0.05). Conclusion: MIR4435-2HG knockdown suppresses the proliferation, migration and invasion of CC cells through regulating the miR-128-3p/MSI2 axis, providing a possible therapeutic strategy for CC.

show abstract

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

<p>Knockdown of MIR4435-2HG Suppresses the Proliferation, Migration and Invasion of Cervical Cancer Cells via Regulating the miR-128-3p/MSI2 Axis in vitro</p>

Wang

Liu

Jiao

et al. 2020

CMAR

View full text Add to dashboard Cite

show abstract

“…Serum miR-125b levels were found to be a useful diagnostic biomarker and a biomarker to predict the responses to chemotherapy in patients with epithelial ovarian cancer 27 . In cervical cancer, it was found that LncRNA CAR10 upregulated PDPK1 to promote cancer development by sponging miR-125b-5p 28 .…”

Section: Discussionmentioning

confidence: 99%

“…Next, we used a bioinformatics website to predict that miR-125b-5p is a shared miRNA of the LncRNA NEAT1 and YES1 genes. LncRNAs regulate gene expression mainly at the epigenetic level, transcription level and posttranscription level 28 . Transcription level and posttranscription level regulation are mainly mediated as molecular sponges, which inhibit the expression of target genes through binding and sponging miRNA 29 .…”

Section: Discussionmentioning

confidence: 99%

MiR-125b-5p Inhibited The Progression of Hepatoblastoma As A Shared miRNA of The lncRNA NEAT1 and YES1

Jin

Chen

Mao

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: microRNAs have been studied widely in hepatoblastoma. However, the role of miR-125b-5p and its relationship with the lncRNA sNEAT1 and YES1 in hepatoblastoma have not been reported previously. We aimed to reveal the role of NEAT1/miR-125b-5p/YES1 in the progression of hepatoblastoma.Methods: We collected tumor tissues and their adjacent tissues from 12 hepatoblastoma patients. qRT-PCR was applied to detect the expression of miR-125b-5p, and the relationship of miR-125b-5p with clinicopathological characteristics was analyzed. Dual luciferase reporter assays and RNA pull down assays were used to identify the relationships among NEAT1, miR-125b-5p and YES1. CCK8, Transwell assays and wound healing assays were used to examine cell viability, invasion and migration. In vivo experiments were also applied to detect the effect of miR-125b-5p on hepatoblastoma.Results: miR-125b-5p was significantly downregulated in hepatoblastoma tissue and cells. The higher the PRETEXT grade, the lower the miR-125b-5p level. NEAT1 could bind to miR-125b-5p and inhibit its expression. miR-125b-5p could target YES1 and inhibit its expression. Overexpression of miR-125b-5p decreased the proliferation, invasion, and migratory ability of hepatoblastoma cells. YES1 could rescue the above effects. At the same time, overexpression of miR-125b-5p resulted in decreased YES1 and tumor growth inhibition in vivo.Conclusion: miR-125b-5p acted as a shared miRNA of NEAT1 and YES1 in hepatoblastoma. Overexpression of miR-125b-5p could target YES1 and inhibit its expression, therefore inhibiting the progression of hepatoblastoma.

show abstract

“…Ge et al reported that CAR10 was upregulated in lung adenocarcinoma tissue, and it could promote lung adenocarcinoma metastasis through down-regulating miR-203 expression (9). Moreover, CAR10 has been con rmed promote cervical cancer development by sponging miR-125b-5p (10). However, till now, the role of CAR10 in PC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

The Inhibition of Long Non-Coding RNA CAR10 and The Regulation of miR-203 Expression Suppresses Cell Viability and Induces Cell Apoptosis in Prostate Cancer

Zhang¹,

Chen²,

Wang³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Prostate cancer (PC) is one of the most common malignant tumors. Recently, it has been reported that long noncoding RNAs (lncRNAs) play key roles in tumor progression. Studies have revealed that long non-coding RNA CAR10 (CAR10) can regulate tumor cell behaviors through sponging miR-203. In this study, we examined the effects of CAR10 in PC cells. Methods: Firstly, real time-quantitative polymerase chain reaction (qRT-PCR) was used to explore CAR10 expression in tumor tissues, peripheral blood of PC patients, and PC cells. We used the dual-luciferase reporter gene assay to analyze the relationship between CAR10 and miR-203. Moreover, flow cytometry, MTT assay, and western blot assay were used to determine cell apoptosis, cell viability, and apoptosis-related protein expression. Results: The results showed that CAR10 expression was remarkably higher in PC samples compared with that of control, and CAR10 regulated miR-203 negatively in PC cells. The qRT-PCR results also showed that miR-203 expression was significantly decreased in PC samples. Moreover, knockdown of CAR10 inhibited PC cell viability and promoted cleaved caspase-3 expression but induced PC cell apoptosis and, reduced pro-caspase-3 expression; miR-203 inhibitor reversed these effects. Conclusion: Our study found that CAR10 is a potential oncogene in PC and suggests that CAR10 inhibition could inhibit PC cell viability but promote PC cell apoptosis through regulating miR-203 expression. Our results show that CAR10 is a potential target for the treatment of PC.

show abstract

LncRNA CAR10 Upregulates PDPK1 to Promote Cervical Cancer Development by Sponging miR-125b-5p

Cited by 25 publications

References 32 publications

<p>Knockdown of MIR4435-2HG Suppresses the Proliferation, Migration and Invasion of Cervical Cancer Cells via Regulating the miR-128-3p/MSI2 Axis in vitro</p>

<p>Knockdown of MIR4435-2HG Suppresses the Proliferation, Migration and Invasion of Cervical Cancer Cells via Regulating the miR-128-3p/MSI2 Axis in vitro</p>

MiR-125b-5p Inhibited The Progression of Hepatoblastoma As A Shared miRNA of The lncRNA NEAT1 and YES1

The Inhibition of Long Non-Coding RNA CAR10 and The Regulation of miR-203 Expression Suppresses Cell Viability and Induces Cell Apoptosis in Prostate Cancer

Contact Info

Product

Resources

About