Mo CJ, Deng XY, Ma RL, Zhu K, Shi L, Li K. Sm-like 5 knockdown inhibits proliferation and promotes apoptosis of colon cancer cells by upregulating p53, CDKN1A and TNFRSF10B. World J Gastrointest Oncol 2024; 16(6): 2716-2726 [DOI: 10.4251/wjgo.v16.i6.2716]
Corresponding Author of This Article
Kang Li, MD, Doctor, Department of Surgical Oncology, The First Affiliated Hospital of Xi’an Jiaotong University, No. 277 Yanta West Road, Yanta District, Xi’an 710061, Shaanxi Province, China. healthlee@xjtu.edu.cn
Research Domain of This Article
Oncology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastrointest Oncol. Jun 15, 2024; 16(6): 2716-2726 Published online Jun 15, 2024. doi: 10.4251/wjgo.v16.i6.2716
Sm-like 5 knockdown inhibits proliferation and promotes apoptosis of colon cancer cells by upregulating p53, CDKN1A and TNFRSF10B
Cai-Jing Mo, Xiao-Yuan Deng, Ru-Lan Ma, Kun Zhu, Lei Shi, Kang Li
Cai-Jing Mo, Xiao-Yuan Deng, Ru-Lan Ma, Kun Zhu, Kang Li, Department of Surgical Oncology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi Province, China
Lei Shi, Department of Infectious Diseases, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi Province, China
Co-corresponding authors: Lei Shi and Kang Li.
Author contributions: Li K and Shi L conceived and supervised the project; Mo CJ, Deng XY, Ma RL and Zhu K contributed to the experiments; Mo CJ and Ma RL wrote the manuscript. All the authors were involved in the study, critically revised the manuscript, and gave final approval.
Supported byNatural Science Basic Research Program of Shaanxi Province, No. 2021JM-256.
Institutional review board statement: This study does not involve any human subjects.
Institutional animal care and use committee statement: This study does not involve any animals.
Conflict-of-interest statement: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Kang Li, MD, Doctor, Department of Surgical Oncology, The First Affiliated Hospital of Xi’an Jiaotong University, No. 277 Yanta West Road, Yanta District, Xi’an 710061, Shaanxi Province, China. healthlee@xjtu.edu.cn
Received: December 27, 2023 Revised: March 18, 2024 Accepted: April 15, 2024 Published online: June 15, 2024 Processing time: 170 Days and 10.5 Hours
Abstract
BACKGROUND
The role of Sm-like 5 (LSM5) in colon cancer has not been determined. In this study, we investigated the role of LSM5 in progression of colon cancer and the potential underlying mechanism involved.
AIM
To determine the role of LSM5 in the progression of colon cancer and the potential underlying mechanism involved.
METHODS
The Gene Expression Profiling Interactive Analysis database and the Human Protein Atlas website were used for LSM5 expression analysis and prognosis analysis. Real-time quantitative polymerase chain reaction and Western blotting were utilized to detect the expression of mRNAs and proteins. A lentivirus targeting LSM5 was constructed and transfected into colon cancer cells to silence LSM5 expression. Proliferation and apoptosis assays were also conducted to evaluate the growth of the colon cancer cells. Human GeneChip assay and bioinformatics analysis were performed to identify the potential underlying mechanism of LSM5 in colon cancer.
RESULTS
LSM5 was highly expressed in tumor tissue and colon cancer cells. A high expression level of LSM5 was related to poor prognosis in patients with colon cancer. Knockdown of LSM5 suppressed proliferation and promoted apoptosis in colon cancer cells. Silencing of LSM5 also facilitates the expression of p53, cyclin-dependent kinase inhibitor 1A (CDKN1A) and tumor necrosis factor receptor superfamily 10B (TNFRSF10B). The inhibitory effect of LSM5 knockdown on the growth of colon cancer cells was associated with the upregulation of p53, CDKN1A and TNFRSF10B.
CONCLUSION
LSM5 knockdown inhibited the proliferation and facilitated the apoptosis of colon cancer cells by upregulating p53, CDKN1A and TNFRSF10B.
Core Tip: Sm-like 5 (LSM5) was highly expressed in tumor tissue and cells of colon cancer. Our study indicated that knockdown of LSM5 had an anti-tumor effect in colon cancer by up-regulating p53, cyclin-dependent kinase inhibitor 1A and tumor necrosis factor receptor superfamily 10B, which providing an important insight on the role of LSM5 in colon cancer development.
