LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells

Mo, Yichao; He, Longguang; Lai, Zeru; Wan, Zhiheng; Chen, Qinshou; Pan, Sibo; Li, Liangfu; Li, Dasheng; Huang, Jun; Xue, Fan; Che, Siyao

doi:10.1186/s13046-018-0831-2

Cited by 46 publications

(31 citation statements)

References 35 publications

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“…For example, lncRNA CDKN2BAS accelerates metastasis in HCC by sponging miR-153-5p and targeting ARHGAP18 [19]. LINC01287/miR-298/STAT3 feedback loop modulates cell growth and the epithelial-to-mesenchymal transition in HCC [20]. LINC01433 facilitates the development of HCC by regulating the miR-1301/STAT3 axis [21].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA FAM83A-AS1 facilitates hepatocellular carcinoma progression by binding with NOP58 to enhance the mRNA stability of FAM83A

2019

Bioscience Reports

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Hepatocellular carcinoma (HCC), as one of the commonest cancers globally, is a primary malignancy in human liver with a characteristic of high mortality rate. Long noncoding RNAs (lncRNAs) are confirmed to be implicated with multiple cancers including HCC. LncRNA FAM83A-AS1 has also been validated as an oncogene in lung cancer, but its mechanism in HCC is poorly understood. Our research is intended to investigate the underlying mechanism of FAM83A-AS1 in HCC. In the present study, we found the abundantly increased expression level of FAM83A-AS1 in HCC tissues and cells. FAM83A-AS1 inhibition hampered cell proliferation, migration and elevated cell apoptosis in HCC. Moreover, FAM83A-AS1 could positively regulate FAM83A, and FAM83A could also promote the progression of HCC. In addition, FAM83A-AS1 and FAM83A were both verified to bind with NOP58, and FAM83A-AS1 enhanced the mRNA stability of FAM83A by binding with NOP58. In rescue assays, the suppressed influence of down-regulated FAM83A-AS1#1 on cell proliferation, migration as well as the accelerated influence of FAM83A-AS1#1 knockdown on cell apoptosis could be partially recovered by overexpression of FAM83A. In conclusion, FAM83A-AS1 facilitated HCC progression by binding with NOP58 to enhance the stability of FAM83A. These findings offer a novel biological insight into HCC treatment.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA FAM83A-AS1 facilitates hepatocellular carcinoma progression by binding with NOP58 to enhance the mRNA stability of FAM83A

2019

Bioscience Reports

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“…According to some other studies (7), miR-15a can affect the proliferation and apoptosis of thyroid cancer cells by regulating AKT. Among those miRNAs, miR-298, located on human chromosome 20q13.32, is related to the proliferation and invasion of tumor cells according to recent studies (8). For example, a study found that miR-298 could affect the proliferation and invasion of ovarian cancer cells by regulating the expression of EZH2 (9).…”

Section: Introductionmentioning

confidence: 99%

Effects of CDK6 regulated by miR‑298 on proliferation and apoptosis of thyroid cancer cells

Li¹,

Liu²,

Zhao

et al. 2020

Oncol Lett

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Effects of CDK6 regulated by miR-298 on proliferation and apoptosis of thyroid cancer cells were explored. Seventy-five cases of thyroid carcinoma and adjacent tissues were collected. The expression levels of miR-298 and CDK6 mRNA in tissues and cells were detected by RT-PCR. In addition, thyroid cancer cells and human normal thyroid cells Nthy-ori3-1 were purchased, with the former transfected with miR-298-mimics, miR-298-inhibitor, miR-NC, si-CDK6, si-NC, Sh-CDK6, Sh-NC to build cell models. Then the expression levels of miR-298 and CDK6 in thyroid cancer tissues and cells were detected by qRT-PCR, and the expression of CDK6, Bax, Bcl-2 and caspase-3 by WB. CCK-8 and flow cytometry were employed to detect cell proliferation and apoptosis, and dual luciferase report was adopted to determine the relationship between miR-298 and CDK6. miR-298 was underexpressed in thyroid cancer, and CDK6 was highly expressed in thyroid cancer. Cell experiments revealed that overexpression of miR-298 or inhibition of CDK6 expression could suppress cell proliferation, promote apoptosis, and significantly increase the expression levels of Bax and caspase-3 proteins, decrease Bcl-2 protein expression, which was contrary to the biological phenotype of cells after inhibition of miR-298 or further overexpression of CDK6. Dual luciferase report confirmed that miR-298 was a targeting site of CDK6. miR-298 can inhibit the proliferation of thyroid cells and promote apoptosis of thyroid cancer cells by regulating the expression of CDK6, which is expected to be a potential target for clinical application.

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“…In addition, it has been reported that lncRNAs are involved in the EMT phenotype. For example, LINC01287 promotes EMT progression to enhance HCC cell invasion via the LINC01287/miR-298/STAT3 feedback loop [32]. LncRNA UCA1 promotes EMT by enhancing Wnt/β-catenin signalling in breast cancer cells [33].…”

Section: Discussionmentioning

confidence: 99%

LINC00355:8 promotes cell proliferation and migration with invasion via the MiR-6777-3p/Wnt10b axis in Hepatocellular Carcinoma

Zhou

Lei

et al. 2020

J. Cancer

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Background: Recent studies have reported that various long non-coding RNAs (lncRNAs) promote hepatocellular carcinoma (HCC) progression, and our previous study indicated that lncRNA LINC00355:8 is overexpressed in HCC. However, the role of LINC00355:8 in HCC is unclear. The primary aim of this study was to explore the biological role of LINC00355:8 in HCC. Methods: Microarray analysis was performed to explore the aberrantly expressed lncRNAs in HCC compared with precancerous tissues. Real-time PCR and in situ hybridization were used to investigate the expression of LINC00355:8 in HCC tissues. CCK8, EdU, colony formation, wound healing and transwell assays were performed to analyse cell proliferation, migration and invasion. A xenograft tumour model was established to analyse the effect of LINC00355:8 on tumour growth in vivo. Luciferase assays were utilized to explore the binding sites between miR-6777-3p and other genes, such as LINC00355:8 and Wnt10b. After cell transfection, the protein expression levels of Wnt10b, β-catenin, E-cadherin, N-cadherin, c-Myc and Snail were determined by Western blotting. Results: The present study revealed that LINC00355:8 was significantly upregulated in HCC, promoted HCC cell proliferation, migration and invasion in vitro and enhanced tumour growth in vivo. LINC00355:8 regulated miR-6777-3p expression by acting as a ceRNA, and the expression of Wnt10b was negatively modulated by miR-6777-3p. Moreover, LINC00355:8 could activate the Wnt/β-catenin signalling pathway and promote EMT progression by inhibiting the miR-6777-3p/Wnt10b interaction in HCC. Conclusion: Our findings indicate that LINC00355:8 activates Wnt10b and promotes HCC progression via the suppression of miR-6777-3p, which may provide novel therapeutic targets for HCC.

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LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells

Cited by 46 publications

References 35 publications

Long noncoding RNA FAM83A-AS1 facilitates hepatocellular carcinoma progression by binding with NOP58 to enhance the mRNA stability of FAM83A

Long noncoding RNA FAM83A-AS1 facilitates hepatocellular carcinoma progression by binding with NOP58 to enhance the mRNA stability of FAM83A

Effects of CDK6 regulated by miR‑298 on proliferation and apoptosis of thyroid cancer cells

LINC00355:8 promotes cell proliferation and migration with invasion via the MiR-6777-3p/Wnt10b axis in Hepatocellular Carcinoma

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