LncRNA HOXA11-AS promotes OSCC progression by sponging miR-98-5p to upregulate YBX2 expression

Niu, Xingyu; Yang, Bin; Liu, Fei; Fang, Qigen

doi:10.1016/j.biopha.2019.109623

Cited by 66 publications

(44 citation statements)

References 26 publications

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“…Long non-coding RNAs (lncRNAs) are a class of non-protein coding transcripts that are >200 nucleotides in length. It has been well reported that lncRNAs play significant roles in cancer biology, including proliferation, invasion, apoptosis and metastasis ( 7 , 8 ). Aberrant expression of lncRNAs has been observed in the occurrence and development of a variety of cancers, suggesting that they may serve as powerful mediators in carcinogenesis ( 9 – 11 ).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of LINC00958 inhibits proliferation, invasion and migration, and promotes apoptosis of colorectal cancer cells by targeting miR‑3619‑5p

et al. 2020

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The aberrant expression of long non-coding RNAs (lncRNAs), including LINC00958, has been demonstrated in several types cancers. The present study aimed to investigate the role of LINC00958 in colorectal cancer (CRC) and identify the possible underlying mechanisms. The expression of LINC00958 and microRNA (miR)-3619-5p was detected in several human CRC cell lines using reverse transcription-quantitative PCR. Then, short hairpin RNA (shRNA)-LINC00958 was transfected into the cells. The results revealed that the expression of LINC00958 was notably upregulated, whereas miR-3619-5p was downregulated in CRC cells. Transfection with shRNA-LINC00958 inhibited the proliferation, invasion and migration of CRC cells. Moreover, the rate of apoptosis was enhanced, accompanied by a decrease in the expression of Bcl-2 and an increase in the expression of Bax and caspase-3. A luciferase reporter assay was conducted to verify the target binding site between LINC00958 and miR-3619-5p. The luciferase reporter assay confirmed that miR-3619-5p could be directly targeted by LINC00958. Furthermore, the miR-3619-5p inhibitor reversed the effects of LINC00958 silencing on proliferation, invasion, migration and apoptosis. Taken together, the findings suggest that the downregulation of LINC00958 suppresses the proliferation, invasion and migration, and promotes the apoptosis of CRC cells by targeting miR-3619-5p in vitro, which provides a theoretical basis and therapeutic strategy for the treatment of CRC.

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Section: Introductionmentioning

confidence: 99%

Downregulation of LINC00958 inhibits proliferation, invasion and migration, and promotes apoptosis of colorectal cancer cells by targeting miR‑3619‑5p

et al. 2020

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“…Furthermore, miR-98-5p can also be regulated by lncRNA. For example, lncRNA HOXA11-AS upregulates YBX2 and accelerates the proliferation and metastasis of oral squamous cell carcinoma (OSCC) through competitively inhibiting miR-98-5p ( 26 ). Further, through bioinformatics analysis, we observed that miR-98-5p is a target of DSCR8, and the targeting relationship between DSCR8 and miR-98-5p was confirmed by dual luciferase reporter assay and RIP experiment.…”

Section: Discussionmentioning

confidence: 99%

A Positive Feedback Loop of lncRNA DSCR8/miR-98-5p/STAT3/HIF-1α Plays a Role in the Progression of Ovarian Cancer

et al. 2020

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Background Accumulating studies have revealed that long non-coding RNA (lncRNA) and microRNA (miRNA) contribute to ovarian cancer (OC). DSCR8 has been found to mediate hepatocellular carcinoma development, while its role in OC remains to be explored. Methods In this study, lncRNA DSCR8 and miR-98-5p expressions in OC tissues and adjacent non-cancer tissues were determined by reverse transcriptase polymerase chain reaction (RT-PCR). Besides, gain-of-function or loss-of-function assays of DSCR8 and miR-98-5p were conducted on OC cell lines SKOV-3 and A2780. Cell proliferation was detected with Cell Counting Kit (CCK)8 and colony formation assay, and western blot was used to test the apoptotic levels of OC cells. Transwell assay was conducted to examine cell invasion, and the epithelial–mesenchymal transition (EMT) of OC cells was tested by western blot. Moreover, luciferase activity assay and RNA immunoprecipitation (RIP) assay were conducted to verify the relationships between DSCR8 and miR-98-5p, miR-98-5p, and signal transducer and activator of transcription 3 (STAT3). Results DSCR8 was remarkedly increased in OC tissues and associated with poorer survival of OC patients. Overexpressing DSCR8 promoted cell proliferation, invasion, and EMT but inhibited apoptosis. On the other hand, miR-98-5p was downregulated in OC tissues and relieved the progression of OC. Moreover, overexpressed DSCR8 increased the levels of STAT3 and hypoxia inducible factor 1 alpha (HIF-1α) and dampened the functions of miR-98-5p on OC. Pharmaceutical intervention of STAT3 and HIF-1α significantly altered the expressions of DSCR8 and miR-98-5p. Conclusion The present results suggested a positive feedback loop of lncRNA DSCR8/miR-98-5p/STAT3/HIF-α axis in the progression of OC.

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“…For instance, HOXA11-AS upregulation has been shown to regulate cell growth via targeting miR-761 in papillary thyroid cancer (31). HOXA11-AS has been demonstrated to play a promoting role in the progression of oral squamous cell carcinoma by sponging miR-98-5p (32). Furthermore, HOXA11-AS has been proven to function as a sponge for miR-125a-5p to upregulate PAdI2 expression and further promote colorectal cancer cell metastasis (33).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA HOXA11‑AS accelerates cell proliferation and epithelial‑mesenchymal transition in hepatocellular carcinoma by modulating the miR‑506‑3p/Slug axis

et al. 2020

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Hepatocellular carcinoma (Hcc) is an aggressively malignant type of cancer with a complex pathogenesis. Multiple studies have identified that lncRNA HOXA11-AS is involved in the development of Hcc. Nevertheless, the pathological mechanisms of HOXA11-AS in the development of Hcc require further investigation. In the present study, the role and underlying mechanisms of HOXA11-AS in HCC were examined. RT-qPCR revealed that HOXA11-AS expression was increased, while that of miR-506-3p was decreased in Hcc tissues and cells compared with that in adjacent non-tumor tissues and normal hepatic cells. dual-luciferase reporter assay and RNA pull-down assay indicated that HOXA11-AS directly interacted with miR-506-3p. miR-506-3p downregulation reversed the inhibitory effects of HOXA11-AS deletion on cell proliferation, invasion and epithelial-mesenchymal transition (EMT), as shown by ccK-8 and Transwell assays, as well as western blot analysis. Bioinformatics analysis and dual-luciferase reporter assay indicated that Slug was a target gene of miR-506-3p. The overexpression of Slug reversed the effects of HOXA11-AS deletion on the viability, invasion and the EMT of Hcc cells. Taken together, the present study demonstrates that HOXA11-AS functions as an oncogene to promote the progression of Hcc via the miR-506-3p/Slug axis, providing a therapeutic target for patients with Hcc.

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LncRNA HOXA11-AS promotes OSCC progression by sponging miR-98-5p to upregulate YBX2 expression

Cited by 66 publications

References 26 publications

Downregulation of LINC00958 inhibits proliferation, invasion and migration, and promotes apoptosis of colorectal cancer cells by targeting miR‑3619‑5p

Downregulation of LINC00958 inhibits proliferation, invasion and migration, and promotes apoptosis of colorectal cancer cells by targeting miR‑3619‑5p

A Positive Feedback Loop of lncRNA DSCR8/miR-98-5p/STAT3/HIF-1α Plays a Role in the Progression of Ovarian Cancer

Long non‑coding RNA HOXA11‑AS accelerates cell proliferation and epithelial‑mesenchymal transition in hepatocellular carcinoma by modulating the miR‑506‑3p/Slug axis

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