» Articles » PMID: 24833469

Knockdown of Response Gene to Complement 32 (RGC32) Induces Apoptosis and Inhibits Cell Growth, Migration, and Invasion in Human Lung Cancer Cells

Overview
Publisher Springer
Specialty Biochemistry
Date 2014 May 17
PMID 24833469
Citations 18
Authors
Affiliations
Soon will be listed here.
Abstract

Response gene to complement 32 (RGC32) is a novel protein originally identified as a cell cycle activator and has been demonstrated to be overexpressed in a variety of human malignancies, including lung cancer. However, the potential role of RGC32 in lung cancer initiation and progression remains to be elucidated. In the present study, RNA interference mediated by plasmid expressing RGC32 short-hairpin RNA (shRNA) was utilized to knockdown RGC32 expression in human lung cancer LTE cells. We found that the mRNA and protein expression levels of RGC32 were significantly decreased in RGC32-specific shRNA-transfected cells in comparison with the untransfected and control shRNA-transfected cells. Furthermore, knockdown of RGC32 dramatically reduced cell proliferation, colony formation, and invasion and migration capacities of LTE cells in vitro. Specific down-regulation of RGC32 caused G0/G1 cell cycle arrest and eventual apoptosis. Meanwhile, Western blot analysis indicated that cells with stably knockdown of RGC32 showed decreased expression levels of Cyclin D1, Cyclin E, Bcl-2, matrix metalloproteinase (MMP)-2, and MMP-9, but increased expression levels of activate caspase-3, Bax, and cleaved poly (ADP-ribose) polymerase (PARP) in comparison with control shRNA-transfected cells. Taken together, our data suggest that RGC32 is involved in tumorigenesis of human lung cancer and may serve as a promising therapeutic target for lung cancer.

Citing Articles

RGCC-mediated PLK1 activity drives breast cancer lung metastasis by phosphorylating AMPKα2 to activate oxidative phosphorylation and fatty acid oxidation.

Cheng S, Wan X, Yang L, Qin Y, Chen S, Liu Y J Exp Clin Cancer Res. 2023; 42(1):342.

PMID: 38102722 PMC: 10722681. DOI: 10.1186/s13046-023-02928-2.


Dpep Inhibits Cancer Cell Growth and Survival via Shared and Context-Dependent Transcriptome Perturbations.

Zhou Q, Greene L Cancers (Basel). 2023; 15(22).

PMID: 38001578 PMC: 10669862. DOI: 10.3390/cancers15225318.


A Novel Prognostic Signature of comprising Nine NK Cell signatures Based on Both Bulk RNA Sequencing and Single-Cell RNA Sequencing for Hepatocellular Carcinoma.

Yu Q, Shi X, Wang H, Zhang S, Hu S, Cai T J Cancer. 2023; 14(12):2209-2223.

PMID: 37576389 PMC: 10414035. DOI: 10.7150/jca.85873.


Diclofenac Disrupts the Circadian Clock and through Complex Cross-Talks Aggravates Immune-Mediated Liver Injury-A Repeated Dose Study in Minipigs for 28 Days.

Selvaraj S, Oh J, Yoon S, Borlak J Int J Mol Sci. 2023; 24(2).

PMID: 36674967 PMC: 9863319. DOI: 10.3390/ijms24021445.


Nonylphenol Promoted Epithelial-Mesenchymal Transition in Colorectal Cancer Cells by Upregulating the Expression of Regulator of Cell Cycle.

Zhang N, Zhang Y, Yin S, Ruan D, He N, Chen X Chem Res Toxicol. 2022; 35(9):1533-1540.

PMID: 36074022 PMC: 9491325. DOI: 10.1021/acs.chemrestox.2c00180.


References
1.
Vlaicu S, Cudrici C, Ito T, Fosbrink M, Tegla C, Rus V . Role of response gene to complement 32 in diseases. Arch Immunol Ther Exp (Warsz). 2008; 56(2):115-22. PMC: 7079747. DOI: 10.1007/s00005-008-0016-3. View

2.
Jemal A, Bray F, Center M, Ferlay J, Ward E, Forman D . Global cancer statistics. CA Cancer J Clin. 2011; 61(2):69-90. DOI: 10.3322/caac.20107. View

3.
Saigusa K, Imoto I, Tanikawa C, Aoyagi M, Ohno K, Nakamura Y . RGC32, a novel p53-inducible gene, is located on centrosomes during mitosis and results in G2/M arrest. Oncogene. 2006; 26(8):1110-21. DOI: 10.1038/sj.onc.1210148. View

4.
Jemal A, Siegel R, Ward E, Hao Y, Xu J, Murray T . Cancer statistics, 2008. CA Cancer J Clin. 2008; 58(2):71-96. DOI: 10.3322/CA.2007.0010. View

5.
Livak K, Schmittgen T . Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods. 2002; 25(4):402-8. DOI: 10.1006/meth.2001.1262. View