Long non-coding RNA TRPM2-AS as a potential biomarker for hepatocellular carcinoma

Xu, Changlu; Huang, Qing; Zhang, C.; Xu, Wanlin; Xu, Guo; Zhao, Xinhan; Liu, X.; Du, Yue

doi:10.1007/s11845-017-1692-y

Cited by 19 publications

(20 citation statements)

References 25 publications

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“…These results demonstrated that TRPM2-AS might work as an oncogene and play crucial roles in glioma progression. Previous studies suggested the promotion of cell apoptosis after the silencing of TRPM2-AS in prostate cancer, liver cancer, and non-small-cell lung cancer Ma et al, 2017;Xu et al, 2018). Whether TRPM2-AS participates in glioma cell apoptosis or not is still a problem in need of further study.…”

Section: Discussionmentioning

confidence: 99%

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TRPM2‐AS inhibits the growth, migration, and invasion of gliomas through JNK, c‐Jun, and RGS4

Bao

Szeto

et al. 2019

Journal Cellular Physiology

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Gliomas are a group of brain cancers with high mortality and morbidity. Understanding the molecular mechanisms is important for the prevention or treatment of gliomas. The present study was to investigate the effects and mechanisms of long noncoding RNA TRPM2-AS in gliomas proliferation, migration, and invasion. We first compared the levels of TRPM2-AS in 111 patients with glioma to that of the normal control group by a quantitative polymerase chain reaction. The results indicated a significant increase of TRPM2-AS in patients with glioma (2.43 folds of control, p = .0135). MTT methods, wound healing assays, transwell analysis, and clone formation analysis indicated the overexpression of TRPM2-AS promoted the proliferation, migration, and invasion of U251 and U87 cells, while downregulation of TRPM2-AS inhibited the cell proliferation, migration, and invasion significantly (p < .05). To further uncover the mechanisms, bioinformatics analysis was conducted on the expression profiles, GSE40687 and GSE4290, from the Gene Expression Omnibus database. One hundred fifty-six genes were differentially expressed in both datasets (FC > 2.0; p = .05). Among these differentially expressed genes, the level of RGS4 messenger RNA was drastically regulated by TRPM2-AS. Further western-blot analysis indicated the increase of RGS4 protein expression and decrease of p-JNK/ JNK and p-c-Jun/c-Jun ratio after TRPM2-AS overexpression. On the other hand, inhibition of TRPM2-AS by small interfering RNA suppressed the expression of RGS4 and promoted the ratios of p-JNK/JNK and p-c-Jun/c-Jun. The present work indicated the mechanisms of the participation of TRPM2-AS in the progression of gliomas might, at least partly, be related to JNK, c-Jun, and RGS4. Our work provided new insights into the underlying mechanisms of glioma cellular functions. K E Y W O R D S glioma, lncRNA, RGS4, TRPM2-AS *Mei-Hua Bao and Qiao-Li Lv contributed equally to this study.

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Section: Discussionmentioning

confidence: 99%

“…TRPM2-AS is an antisense lncRNA mapped to 44 658 901-44 669 874 position of TRPM2 gene (Orfanelli et al, 2008). It was demonstrated to be an oncogene for non-small-cell lung cancer, prostate cancer, and hepatocellular carcinoma (Huang et al, 2017;Orfanelli et al, 2015;Xu et al, 2018). However, its effects in gliomas are unknown.…”

Section: Discussionmentioning

confidence: 99%

TRPM2‐AS inhibits the growth, migration, and invasion of gliomas through JNK, c‐Jun, and RGS4

Bao

Szeto

et al. 2019

Journal Cellular Physiology

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“…In addition, TRPM2-AS was reported to be up-regulated in breast cancer to promote uncontrollable proliferation and weaken breast cancer cells' apoptosis through binding with miR-140-3p [14]. Besides, TRPM2-AS was up-regulated in hepatocellular carcinoma (HCC) tissues than in normal adjacent tissues, and it had a significant correlation with tumor size, differentiation, and the prognosis outcome of HCC patients [16]. Compared with previous studies, our results had the similar conclusion that TRPM2-AS was up-regulated in BLCA to promote the cell viability and cell proliferation, and inhibit cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…The host gene of TRPM2-AS, transient receptor potential cation channel subfamily M member 2 antisense RNA, consists of 3 exons and locates at chromosome 21q22.3. TRPM2-AS was first discovered to be up-regulated in melanoma in 2008 [10], and it was gradually found that to be a cancer-promoting gene in more other tumors including reproductive system tumors, digestive system tumors and respiratory system tumors [11][12][13][14][15][16][17]. Yet, there have been no researches exploring how TRPM2-AS implements a marked effect 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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“…10,11 TRPM2-AS locates at human chr21q22.3, and consists of 875 nucleotides with three exons in the translation template. 12 TRPM2-AS has been revealed to be upregulated and involved in the progression of melanoma, 12 non-small cell lung cancer, 13,14 hepatocellular carcinoma, 15 and prostate cancer. [16][17][18] The expression status and function of TRPM2-AS were still in osteosarcoma.…”

Section: Introductionmentioning

confidence: 99%

Transient receptor potential melastatin 2–antisense RNA is overexpresed in osteosarcoma and regulates cell proliferation and apoptosis

Geng

Ming

2018

J of Cellular Biochemistry

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Accumulating evidence suggested that transient receptor potential melastatin 2–antisense RNA (TRPM2‐AS) played crucial roles in the progression of human cancers. However, the role of TRPM2‐AS was still unknown in osteosarcoma. The aim of this study was to explore the clinical significance of TRPM2‐AS in osteosarcoma patients, and determine the role of TRPM2‐AS on osteosarcoma cell proliferation and apoptosis. In our results, we identified a novel oncogenic long noncoding RNA TRPM2‐AS, which was overexpressed in osteosarcoma tissues and cells, and correlated with advanced Enneking stage, large tumor size and high histological grade in osteosarcoma cases. Survival analysis indicated that osteosarcoma patients with high TRPM2‐AS expression had an obviously shorter overall survival time than those with low TRPM2‐AS expression. Loss‐of‐function studies suggested that suppression of TRPM2‐AS expression inhibited osteosarcoma cell proliferation and induced cell apoptosis through upregulating cleaved caspase‐3 and cleaved caspase‐9 expression. In conclusion, TRPM2‐AS acts as an oncogenic long noncoding RNA and predicts poor prognosis in osteosarcoma.

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Long non-coding RNA TRPM2-AS as a potential biomarker for hepatocellular carcinoma

Cited by 19 publications

References 25 publications

TRPM2‐AS inhibits the growth, migration, and invasion of gliomas through JNK, c‐Jun, and RGS4

TRPM2‐AS inhibits the growth, migration, and invasion of gliomas through JNK, c‐Jun, and RGS4

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

Transient receptor potential melastatin 2–antisense RNA is overexpresed in osteosarcoma and regulates cell proliferation and apoptosis

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