LINC01006 promotes cell proliferation and metastasis in pancreatic cancer via miR-2682-5p/HOXB8 axis

Zhang, Luyang; Wang, Yunjian; Zhang, Ling; You, Guohua; Li, Congyu; Meng, Bo; Zhou, Minghe; Zhang, Min

doi:10.1186/s12935-019-1036-2

Cited by 34 publications

(31 citation statements)

References 39 publications

(43 reference statements)

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“…Then, RT-qPCR was applied to estimate the relative expression of those candidate miRNAs, and finally, miR-497-5p gained our attention with the most obvious differential expression. As presented in previous studies, miR-497-5p is associated with multiple cancer development, such as colorectal cancer, breast cancer, and pancreatic cancer [37-39]. In our research, bioinformatic tools were used to hypothesize the binding site between CASC9 and miR-497-5p in BC.…”

Section: Discussionmentioning

confidence: 80%

CASC9 Facilitates Cell Proliferation in Bladder Cancer by Regulating CBX2 Expression

Huo

Tan

Chen

2020

Nephron

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Background: As the seventh most common urologic carcinoma worldwide, approximately 430,000 patients are diagnosed with bladder cancer (BC) every year. Increasing evidence indicates that long noncoding RNAs (lncRNAs) play crucial roles in the progression of BC. Objectives: This study is aimed to explore the function and mechanism of CASC9 in BC. Methods: Bioinformatics analysis and experiments including RT-qPCR, luciferase reporter, Cell Counting Kit-8 assay, Western blot, RNA immunoprecipitation assay, and TU-NEL staining were applied to explore the function and mechanism of CASC9 in BC tissues and cell lines. Results: Our study demonstrated that CASC9 was upregulated in BC tissues and cell lines. Moreover, we found that CASC9 knockdown notably decreased proliferation while increased apoptotic rate in BC cells. Mechanistically, bioinformatics prediction and following experiments indicated that CASC9 worked as a competing endogenous RNA (ceRNA) of CBX2 through sponging miR-497-5p. Meanwhile, we recognized that CASC9 and miR-497-5p negatively regulated each other in a mutual way. Furthermore, we found that miR-497-5p shared binding site with CBX2. In addition, miR-497-5p could negatively regulated CBX2, while CASC9 could positively regulated CBX2. Rescue assays reveled that CBX2 overexpression could reversed the reduction of cell proliferation or the enhancement of cell apoptosis induced by CASC9 suppression. Conclusions: Our study manifests the first evidence that CASC9 serves as an oncogene in BC and accelerates cell proliferation by modulating miR-497-5p/CBX2 axis. The present study may provide a cogitable target for BC therapy.

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Section: Discussionmentioning

confidence: 80%

CASC9 Facilitates Cell Proliferation in Bladder Cancer by Regulating CBX2 Expression

Huo

Tan

Chen

2020

Nephron

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“…For instance, lncRNA NORAD promoted cell proliferation by competitively binding with miR-155-5p [14]. LINC00339 accelerated cell metastasis in pancreatic cancer by sponging miR-497-5p and modulating IGF1R [15]. FOXO1 suppressed cell metastasis by down-regulating AKT and inhibited lung cancer [16].…”

Section: Introductionmentioning

confidence: 99%

LncRNA LINC00668 promotes cell proliferation, migration, invasion ability and EMT process in hepatocellular carcinoma by targeting miR-532-5p/YY1 axis

2020

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Liver cancer is now one of the most lethal and commonest cancers in the world, among which over 90% is hepatocellular carcinoma (HCC). Recent studies have confirmed long non-coding RNAs (lncRNAs) are implicated in carcinogenesis. It has been reported lncRNA LINC00668 serves as an oncogene in several cancers. However, the mechanism where LINC00668 regulates HCC is still unclear. qRT-PCR analysis was adopted to detect the expression of relative RNAs. Cytoplasmic and nuclear RNA fraction analysis was conducted to verify the underlying molecular mechanism. Cell colony formation was carried out to test cell colony formation ability and transwell assays were performed to testify cell migratory and invaded abilities. Relevant protein expression level was measured by Western blot assay. LINC00668 was significantly up-regulated in HCC tissues and cell lines. LINC00668 knockdown inhibited cell proliferative, migratory and invasion abilities and slowed down the epithelial–mesenchymal transition (EMT) process. Mechanistically, LINC00668 positively modulates the expression of YY1 by competitively binding to miR-532-5p. It was revealed that LINC00668 up-regulation accelerated cell proliferation and motility in HCC and suggested LINC00668 could be a potential therapeutic target for HCC.

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“…LINC00339 level was high in PC tissues and cell models. In detail, LINC00339 was reported to enhance cell proliferation and metastasis of PC (Zhang et al 2019a). Linc-ROR was increased in PC tissues, and ectopic expression of linc-ROR facilitated proliferation, migration and invasion in PC (Zhan et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA MCM3AP-AS1 promotes growth and migration through modulating FOXK1 by sponging miR-138-5p in pancreatic cancer

Yang

Sun

Guo

et al. 2019

Mol Med

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Background: Pancreatic cancer (PC) is a type of malignant gastrointestinal tumor. Long non-coding RNA MCM3AP antisense RNA 1 (MCM3AP-AS1) has been reported to stimulate proliferation, migration and invasion in several types of tumors. However, the role of MCM3AP-AS1 in PC remains unclear.Methods: MCM3AP-AS1, microRNA miR-138-5p (miR-138-5p) and FOXK1 levels were detected using quantitative real time PCR. Cell proliferation, migration and invasion were analyzed. Dual luciferase reporter assay was used to confirm the relationship between MCM3AP-AS1 and miR-138-5p, between miR-138-5p and FOXK1. Protein levels were identified using western blot analysis. Results: MCM3AP-AS1 overexpression promoted proliferation, migration and invasion in PC cells. MCM3AP-AS1 silencing showed a suppressive effect on cell growth in PC cells. Moreover, MCM3AP-AS1 knockdown suppressed tumor growth in mice. Dual luciferase reporter assay demonstrated MCM3AP-AS1 could sponge microRNA-138-5p (miR-138-5p), and FOXK1 could bind with miR-138-5p. Positive correlation between MCM3AP-AS1 and FOXK1 was testified, as well as negative correlation between miR-138-5p and FOXK1. MCM3AP-AS1 promoted FOXK1 expression by targeting miR-138-5p, and MCM3AP-AS1 facilitated growth and invasion in PC cells by FOXK1. Conclusion: MCM3AP-AS1 promoted growth and migration through modulating miR-138-5p/FOXK1 axis in PC, providing insights into MCM3AP-AS1/miR-138-5p/FOXK1 axis as novel candidates for PC therapy from bench to clinic.

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LINC01006 promotes cell proliferation and metastasis in pancreatic cancer via miR-2682-5p/HOXB8 axis

Cited by 34 publications

References 39 publications

CASC9 Facilitates Cell Proliferation in Bladder Cancer by Regulating CBX2 Expression

CASC9 Facilitates Cell Proliferation in Bladder Cancer by Regulating CBX2 Expression

LncRNA LINC00668 promotes cell proliferation, migration, invasion ability and EMT process in hepatocellular carcinoma by targeting miR-532-5p/YY1 axis

Long non-coding RNA MCM3AP-AS1 promotes growth and migration through modulating FOXK1 by sponging miR-138-5p in pancreatic cancer

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