Long non-coding RNA LINC00858 promotes cells proliferation, migration and invasion by acting as a ceRNA of miR-22-3p in colorectal cancer

Sha, Qian-Kun; Chen, Lin; Xi, Jia-Zhuang; Song, Hang

doi:10.1080/21691401.2018.1544143

Cited by 53 publications

(42 citation statements)

References 30 publications

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“…Xiong, X et al [27] demonstrated that linc00052 functioned as a tumor suppressor via negatively regulating miR-330-3p in pancreatic cancer. Instead, linc00858 exerted its function through the suppression of miR-22-3p to promote cells proliferation, migration and invasion [28]. Thus, it is concluded that miRNAs can become a direct target of linc RNAs to exert its effect on the development of cancer.…”

Section: Discussionmentioning

confidence: 99%

Up-regulated Linc00472 suppresses development of lung cancer cell via inhibition of MiR-196b-5p

Mao¹,

Zhou²,

Li³

et al. 2019

Bioscience, Biotechnology, and Biochemistry

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The role of linc00472 in lung cancer (LC) has been rarely reported. We aimed to study the role of linc00472 in LC progression. Expressions of linc00472 and miR-196b-5p in LC cell lines were measured by qRT-PCR. The targeting relationship between linc00472 and miR-196b-5p was determined by Starbase and dual-luciferase reporter. The viability, migration, invasion, and apoptosis of LC cells were determined using CCK-8 assay, scratch test, transwell assay, and flow cytometry, respectively. The levels of epithelial-to-mesenchymal transition (EMT)-related proteins and apoptosis-related proteins in LC cells were determined by western blot. Downregulated linc00472 was observed in five LC cell lines. Linc00472 overexpression suppressed viability, migration, invasion and EMT process, but elevated apoptotic rate in LC cells. MiR-196b-5p mimic promoted viability, migration, invasion, and EMT process, but decreased apoptotic rate, which was reversed by up-regulated linc00472. Linc00472 functioned as a cancer suppressor via negatively regulating miR-196b-5p of LC cells.

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Section: Discussionmentioning

confidence: 99%

Up-regulated Linc00472 suppresses development of lung cancer cell via inhibition of MiR-196b-5p

Mao¹,

Zhou²,

Li³

et al. 2019

Bioscience, Biotechnology, and Biochemistry

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“…31 Sha et al showed that LINC00858 induced colorectal cancer development via acting as a ceRNA of miR-22-3p. 32 In lung adenocarcinoma, lncRNA DGCR5 contributed to cancer progression through sponging miR-22-3p. 33 A recent study suggested that miR-22 suppressed lung cancer cell EMT and invasion via targeting Snail.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NNT‐AS1 promotes non‐small cell lung cancer progression through regulating miR‐22‐3p/YAP1 axis

Zhang

Xia

2020

Thoracic Cancer

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Background Lung cancer is the leading cause of cancer‐related mortality worldwide. Studies have demonstrated that long noncoding RNA nicotinamide nucleotide transhydrogenase‐antisense RNA1 (NNT‐AS1) functioned as an oncogene in most malignancies, including non‐small cell lung cancer (NSCLC). This study aimed to investigate the underlying mechanisms of NNT‐AS1 in NSCLC progression. Methods The levels of NNT‐AS1, miR‐22‐3p and Yes‐associated protein (YAP1) were detected by qRT‐PCR in NSCLC tissues and cells. Kaplan‐Meier analysis was conducted to analyze the correlation between NNT‐AS1 expression and overall survival of NSCLC patients. Cell proliferation was evaluated by MTT assay. Cell migration and invasion were assessed using transwell assay. The protein levels of YAP1 and EMT‐related proteins were detected by western blot. The molecular mechanism was predicted by starBase2.0 and validated by dual‐luciferase reporter assay or RNA pull‐down assay. Xenograft analysis was carried out to analyze tumor growth in vivo. Results We found that the levels of NNT‐AS1 and YAP1 were enhanced, while miR‐22‐3p expression was decreased in NSCLC tissues and cells. High NNT‐AS1 expression was correlated with poor prognosis. NNT‐AS1 knockdown impeded proliferation, migration, invasion and EMT of NSCLC cells. NNT‐AS1 targeted miR‐22‐3p, and YAP1 was a target of miR‐22‐3p in NSCLC cells. Furthermore, NNT‐AS1 facilitated the progression of NSCLC by regulating miR‐22‐3p/YAP1 axis. NNT‐AS1 knockdown repressed tumor growth in vivo. Conclusion NNT‐AS1 facilitated proliferation, migration, invasion and EMT of NSCLC cells by sponging miR‐22‐3p and regulating YAP1 expression, which might provide a potential biomarker and therapeutic target for NSCLC.

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“…In gastric cancer, miR-22-3p was reported to be regulated by lncRNA CTC-497E21.4 thus regulating NET1 expression to suppress the malignant development of gastric cancer [44]. Moreover, LINC00858 acted through ceRNA network to suppress miR-22-3p, thereby regulating the down-stream effector, YWHAZ, to strengthen the progression of colorectal cancer [25]. We herein validated the regulatory relationship between miR-22-3p and TRPM2-AS, and the latter promoted BLCA by suppressing the former.…”

Section: Discussionmentioning

confidence: 99%

“…Among them, miRNAs have been frequently referred to important gene expression regulators and play essential roles in cancer progression. During the last three years, miR-22-3p's role in BLCA started to emerge and be studied, although it had been discovered to act as a tumor suppressor in neoplasms that occur in reproductive system, digestive system and respiratory system before [21][22][23][24][25][26][27]. But it is no research regarding the involvement of miR-22-3p in a lncRNA-related interactome complex in BLCA.…”

Section: Introductionmentioning

confidence: 99%

TRPM2-AS promotes bladder cancer-genesis by targeting miR-22-3p thus releasing GINS2 mRNA

Tian¹,

Guan²,

Su³

et al. 2020

Preprint

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Background: We aimed to study the effects of lncRNA TRPM2-AS in bladder cancer (BLCA) by interacting with its downstream effectors miR-22-3p and GINS2 mRNA.Methods: Online bioinformatic tools were used to identify the key lncRNA, miRNA and mRNA of interest in BLCA. TRPM2-AS, miR-22-3p and GINS2 mRNA expression was measured by qRT-PCR in bladder tissues and selected cell lines. Subcellular localization of TRPM2-AS in T24 and 5637 cell lines was identified using a cellular fractionation method. Luciferase reporter assay, RIP assay and RNA pull-down assay were employed to validate the direct binding relationship between TRPM2-AS, miR-22-3p and GINS2 mRNA. Cell viability, proliferation and apoptosis were measured by a series of cell functional experiments in T24 and 5637 cells.Results: TRPM2-AS was primarily located in cell cytoplasm and significantly up-regulated in BLCA tissues and cell lines. TRPM2-AS knockdown significantly inhibited cell viability and proliferation, but promoted cell apoptosis. miR-22-3p, a significant downstream target of TRPM2-AS, showed a lower expression level in BLCA tissues and cell lines. miR-22-3p inhibition resulted in a significant enhancement of BLCA cancer cell phenotypes. Lastly, GINS2 mRNA was a downstream target of miR-22-3p, and was significantly up-regulated in BLCA. The knockdown of GINS2 led to a significant suppression of BLCA cancer cell phenotypes.Conclusions: TRPM2-AS was a tumor promoter and fulfilling its role through binding to miR-22-3p to increase GINS2 expression. This novel interactome in BLCA might become a new therapy in BLCA.

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Long non-coding RNA LINC00858 promotes cells proliferation, migration and invasion by acting as a ceRNA of miR-22-3p in colorectal cancer

Cited by 53 publications

References 30 publications

Up-regulated Linc00472 suppresses development of lung cancer cell via inhibition of MiR-196b-5p

Up-regulated Linc00472 suppresses development of lung cancer cell via inhibition of MiR-196b-5p

LncRNA NNT‐AS1 promotes non‐small cell lung cancer progression through regulating miR‐22‐3p/YAP1 axis

TRPM2-AS promotes bladder cancer-genesis by targeting miR-22-3p thus releasing GINS2 mRNA

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