LncRNA THOR increases the stemness of gastric cancer cells via enhancing SOX9 mRNA stability

Hu, Song; Xu, Yixin; Shi, Linseng; Xu, Teng; Fan, Ruizhi; Cao, Meng; Xu, Wei; Song, Jun

doi:10.1016/j.biopha.2018.09.057

Cited by 64 publications

(59 citation statements)

References 30 publications

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“…Metastasis-associated in colon cancer-1 antisense RNA (MACC1-AS1) could promote stemness of GC via fatty acid oxidation 43 . Knockdown of lncRNA testis-associated highly conserved oncogenic long non-coding RNA (THOR) inhibited the stemness of GC 44 . This study first revealed that xxx; FEZF1-AS1: FEZ family zinc finger 1 antisense RNA 1; H&E: hematoxylin and eosin; HMGA2: high-mobility group AT-hook 2; mRNA: messenger ribonucleic acid; Nanog: nanog homeobox; Oct: octamer-binding transcription factor; qRT-PCR: quantitative reverse transcription PCR; SOX: sex-determining region Y-Box transcription factor.…”

Section: Discussionmentioning

confidence: 99%

LncRNA FEZF1-AS1 Modulates Cancer Stem Cell Properties of Human Gastric Cancer Through miR-363-3p/HMGA2

Hui

Yang

et al. 2020

Cell Transplant

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Gastric cancer (GC) is a leading cause of cancer-related death with poor prognosis. Growing evidence has shown that long noncoding ribonucleic acid (lncRNA) FEZ family zinc finger 1 antisense RNA 1(FEZF1-AS1), an “oncogene,” regulates tumor progression and supports cancer stem cell. However, the tumorigenic mechanism of FEZF1-AS1 on gastric cancer stem cell (GCSC) is yet to be investigated. Here, we discovered that FEZF1-AS1 was upregulated in GC tissues and cell lines. Knockdown of FEZF1-AS1 inhibited sphere formation and decreased expression of stem factors and markers. Moreover, FEZF1-AS1 silence also suppressed cell proliferation, viability, invasion, and migration of GCSCs. MiR-363-3p is used as a target of FEZF1-AS1, because its expression was suppressed by FEZF1-AS1 in GCSCs. FEZF1-AS1 could sponge miR-363-3p and increased the expression of high-mobility group AT-hook 2 (HMGA2). The expression of FEZF1-AS1 and miR-363-3p, as well as that of miR-363-3p and HMGA2, was negatively correlated in GC tissues. Finally, FEZF1-AS1 contributed to promotion of GCSCs progression partially through inhibition of miR-363-3p. Subcutaneous xenotransplanted tumor model revealed that silence of FEZF1-AS1 suppressed in vivo tumorigenic ability of GSCS via downregulation of HMGA2. In general, our findings clarified the critical regulatory role of FEZF1-AS1/miR-363-3p/HMGA2 axis in GCSC progression, providing a potential therapeutic target for GC.

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Section: Discussionmentioning

confidence: 99%

LncRNA FEZF1-AS1 Modulates Cancer Stem Cell Properties of Human Gastric Cancer Through miR-363-3p/HMGA2

Hui

Yang

et al. 2020

Cell Transplant

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“…LncRNAs could function by different pathways, such as lncRNAs serve as the protein co‐activators or co‐repressors, and thus the co‐regulators of mRNA and DNA . Recent studies have revealed the ceRNA roles of lncRNAs .…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA ANRIL enhances mitochondrial function of hepatocellular carcinoma by regulating the MiR‐199a‐5p/ARL2 axis

Bao

Wei

et al. 2019

Environmental Toxicology

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Although the roles of long non-coding RNA (lncRNA) ANRIL (Antisense non-coding RNA in the INK4A locus) have been established in various tumors, its roles in mitochondrial metabolic reprogramming of hepatocellular carcinoma (HCC) cells are still unclear. This work aims to explore lncRNA ANRIL roles in regulating the mitochondrial metabolic reprogramming of liver cancer cells. First, we found that lncRAN ANRIL expression was significantly increased in HCC tissues or cells compared with the normal adjacent tissues and normal tissues or cells. Functional experiment showed that overexpression of lncRNA ANRIL promoted mitochondrial function in HCC cells, evident by the increased mitochondrial DNA copy numbers, ATP (Adenosine triphosphate) level, mitochondrial membrane potential, and the expression levels of mitochondrial markers, while ANRIL knockdown exerted the opposite effects. Mechanistically, lncRNA ANRIL acted as a competing endogenous RNA to increase ARL2 (ADP-ribosylationfactor-like 2) expression via sponging miR-199a-5p. Notably, the miR-199a-5p/ARL2 axis is necessary for ANRIL-mediated promoting effects on HCC cell mitochondrial function. This work reveals a novel ANRIL-miR-199a-5p-ARL2 axis in HCC cell progression, which might provide potential targets for HCC treatment. K E Y W O R D SANRIL, ARL2, ceRNA, hepatocellular carcinoma, lncRNA, miR-199a-5p

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“…As described previously [28], in situ cell death detection kit (Roche, Penzberg, Upper Bavaria, Germany) was utilized to identify the apoptotic cells under the manufacturer's protocols. Nuclei were stained by DAPI.…”

Section: Terminal Deoxynucleotidyl Transferase Dutp Nick End Labelingmentioning

confidence: 99%

TMPO-AS1 promotes cell proliferation of thyroid cancer via sponging miR-498 to modulate TMPO

Feng

Zhang

et al. 2020

Cancer Cell Int

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Background: Thyroid cancer (TC) is the most frequent endocrine malignancy. Long noncoding RNAs (lncRNAs) have been confirmed to act as significant roles in tumor development. The role of lncRNA TMPO-AS1 in TC is still unclear, so it remains to be explored. The aim of the research is to investigate the role and regulatory mechanism of TMPO-AS1 in TC. Methods: TMPO-AS1 and TMPO expression in TC tumors and cells was detected by TCGA database and QRT-PCR assay respectively. CCK-8, EDU, TUNEL and western blot assays were conducted to identify the biological functions of TMPO-AS1 in TC. Luciferase reporter and RNA pull down assays were conducted to measure the interaction among TMPO-AS1, TMPO and miR-498. Results: TMPO-AS1 was overexpressed in TC tissues and cell lines. Knockdown of TMPO-AS1 suppressed cell growth and accelerated cell apoptosis in TC. Furthermore, downregulation of TMPO-AS1 suppressed TMPO expression in TC. The data suggested that TMPO expression was upregulated in TC tissues and cell lines and was positively correlated with TMPO-AS1 expression in TC. Furthermore, the expression of miR-498 presented low expression in TC cells. And miR-498 expression was negatively regulated by TMPO-AS1, meanwhile, TMPO expression was negatively regulated by miR-498 in TC cells. Besides, it was confirmed that TMPO-AS1 could bind with miR-498 and TMPO in TC cells. In addition, it was validated that TMPO-AS1 elevated the levels of TMPO via sponging miR-498 in TC cells. Conclusions: TMPO-AS1 promotes cell proliferation in TC via sponging miR-498 to modulate TMPO.

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LncRNA THOR increases the stemness of gastric cancer cells via enhancing SOX9 mRNA stability

Cited by 64 publications

References 30 publications

LncRNA FEZF1-AS1 Modulates Cancer Stem Cell Properties of Human Gastric Cancer Through miR-363-3p/HMGA2

LncRNA FEZF1-AS1 Modulates Cancer Stem Cell Properties of Human Gastric Cancer Through miR-363-3p/HMGA2

Long non‐coding RNA ANRIL enhances mitochondrial function of hepatocellular carcinoma by regulating the MiR‐199a‐5p/ARL2 axis

TMPO-AS1 promotes cell proliferation of thyroid cancer via sponging miR-498 to modulate TMPO

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