Article Sidebar
Published:
Oct 6, 2024DOI:
10.4314/ahs.v24i3.24Keywords:
Article Details
While African Health Sciences has been freely accessible online there have been questions on whether it is Open Access or not. We wish to clearly state that indeed African Health Sciences is Open Access. There are key issues regarding Open Access needing clarification for avoidance of doubt:
- 1. Henceforth, papers in African Health Sciences will be published under the CC BY (Creative Commons Attribution License) 4.0 International. See details on https://creativecomons.org/)
- 2. The copyright owners or the authors grant the 3rd party (perpetually and in advance) the right to disseminate, reproduce, or use the research papers in part or in full, format/medium as long as:
- No substantive errors are introduced in the process
- Attribution of authorship and correct citation details are given
- The referencing details are not changed.
Should the papers be reproduced in part, this must be clearly stated.
- 3. The papers will be freely and universally accessible online in an easily readable format such as XML in at least one widely recognized open access repository such as PUBMED CENTRAL.
B. ABRIDGED LICENCE AGREEMENT BETWEEN AUTHORS AND African Health Sciences
I submitted my manuscript to African Health Sciences and would like to affirm that:
1.0 I am authorized by my co-authors to enter into these arrangements.
2.0 I guarantee, on behalf of self and co-authors:
- That the paper is original, and has not been published in any other peer-reviewed journal; nor is it under consideration by other journal (s). It does not infringe existing copyright or any other person’s rights
- That we are/I am the sole author(s) of the paper and with authority to enter into this agreement. My granting rights to African Health Sciences is not in breach of any other obligation
- That the paper contains nothing unlawful, or libelous. Nor anything that would constitute a breach of contract, confidence or commitment given to secrecy, if published
- That I/we have taken care to ensure the integrity of the article.
3.0 I and all co-authors, agree that the paper, if accepted for publication, shall be licensed under the Creative Commons Attribution License 4.0. (see https://creativecommons.org/)
Main Article Content
MiRNA-153 attenuates progression of non-small cell lung cancer through targeting positive regulatory/SET domain 2
Abstract
Background: To explore whether micro ribonucleic acid (miR)-153 regulates positive regulatory/SET domain 2 (PRDM2) in a targeted manner and affects the proliferation and apoptosis of non-small cell lung cancer (NSCLC) A549 cells.
Methodology: The expressions of miR-153 and PRDM2 in NSCLC tissues and A549 cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). TargetScan was utilized to predict miR-153 target genes. Methyl thiazolyl tetrazolium (MTT) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays were carried out to study the cell proliferation and apoptosis. Western blotting was performed to examine the changes in the proteins in the Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling pathway following the miR-153 overexpression.
Results: The expression of miR-153 was decreased and that of PRDM2 was increased in NSCLC tissues and cells. Target genes regulated by miR-153 participated in self-vascular development, miRNA metabolic process and the Wnt signaling pathway. The overexpression of miR-153 led to an obvious reduction in the proliferation ability of A549 cells, a notable increase in apoptotic cells, and significant decreases in phosphorylated (p)-JAK2 and p-STAT3 proteins. Dual-luciferase reporter gene assay revealed that miR-153 could directly modulate the expression level of PRDM2.
Conclusion: MiR-153 directly targets PRDM2 and affects A549 cell proliferation and apoptosis through the JAK/STAT pathway.
Keywords: Non-small cell lung cancer; miR-153; positive regulatory/SET domain 2; Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling pathway.
