Research Paper Volume 15, Issue 8 pp 2877—2890
LINC01296 promotes proliferation of cutaneous malignant melanoma by regulating miR-324-3p/MAPK1 axis
- 1 Department of General Surgery, Gaoyou People’s Hospital, Yangzhou 225600, China
- 2 Department of Dermatology, The First People’s Hospital of Lianyungang, Lianyungang Clinical Medical College of Nanjing Medical University, Lianyungang 222002, China
- 3 Department of General Medicine, The First People’s Hospital of Lianyungang, Lianyungang Clinical Medical College of Nanjing Medical University, Lianyungang 222002, China
Received: July 26, 2022 Accepted: November 21, 2022 Published: December 2, 2022
https://doi.org/10.18632/aging.204413How to Cite
Copyright: © 2023 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
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 real-time 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-NC-xenografted 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.