Prognostic value of long non-coding RNA 01296 expression in human solid malignant tumours: a meta-analysis

Dai, Chen; Dai, Chenguang; Ni, Hao; Xu, Zhihua

doi:10.1136/postgradmedj-2019-136684

Cited by 1 publication

(1 citation statement)

References 38 publications

(60 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nowadays, increasing researches have reported that a number of lncRNAs might play multiple functions in the initiation and progression of CMM [ 15 , 16 ]. LINC01296 was found to be aberrantly expressed in several malignancies, including hepatocellular carcinoma, osteosarcoma and oral squamous cell carcinoma, and LINC01296 could also regulate tumorigenesis and progression of cancers [ 17 ]. We also observed aberrant expression of LINC01296 in CMM by GEPIA data analysis.…”

Section: Introductionmentioning

confidence: 99%

LINC01296 promotes proliferation of cutaneous malignant melanoma by regulating miR-324-3p/MAPK1 axis

Wang¹,

Luo

Zhang³

et al. 2022

Aging

View full text Add to dashboard Cite

Objective: To investigate the functions and potential molecular mechanism of LINC01296 regarding the progression of cutaneous malignant melanoma (CMM) by the regulation of miR-324-3p/MAPK1 axis. Methods: The candidate differential lncRNAs of CMM were selected from GEPIA database, and quantitative realtime PCR (qRT-PCR) was utilized to assess the expression level of LINC01296 in human CMM tissues and cell lines. Cell proliferation assay, Colony formation assay, Ethynyl-2'-deoxyuridine (EDU) assay in vitro and tumorigenicity assays in nude mice in vivo were performed to examine the functions of LINC01296. Bioinformatics analysis, luciferase reporter assay and rescue experiments were also gained an insight into the underlying mechanisms of LINC01296 in CMM cell lines by miR-324-3p/MAPK1 axis. Results: In this study, the up-regulation of LINC01296 was found in CMM tissues and cell lines. Functionally, the over-expression of LINC01296 promoted the proliferation in CMM cell lines. In addition, immunochemistry analysis confirmed that the levels of MAPK1 and Ki-67 in sh-LINC01296-xenografted tumors was weaker than that in sh-NCxenografted tumors. Then, bioinformatics analysis confirmed that LINC01296 interacted with miR-324-3p. Further investigations showed that MAPK1, which collected from the potential related genes of LINC01296, was the conjugated mRNA of miR-324-3p by luciferase reporter assay. Finally, the rescue experiments suggested the positive regulatory association among LINC01296 and MAPK1, which showed that MAPK1 could reverse the promoting-effect of LINC01296 in CMM cells in vitro. Conclusions: Therefore, our findings provided insight into the mechanisms of LINC01296 via miR-324-3p/MAPK1 axis in CMM, and revealed an alternative target for the diagnosis and treatment of CMM.

show abstract

Section: Introductionmentioning

confidence: 99%