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Luo H, Xu C, Ge B, Wang T. CASC1 Expression in Bladder Cancer Is Regulated by Exosomal miRNA-150: A Comprehensive Pan-Cancer and Bioinformatics Study. COMPUTATIONAL AND MATHEMATICAL METHODS IN MEDICINE 2022; 2022:8100325. [PMID: 35836922 PMCID: PMC9276518 DOI: 10.1155/2022/8100325] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 03/03/2022] [Revised: 05/30/2022] [Accepted: 06/01/2022] [Indexed: 11/18/2022]
Abstract
This study explored the role of cancer susceptibility 1 (CASC1) in tumorigenesis and development as well as the key pathways affecting bladder cancer progression. CASC1 was examined in various normal tissues in humans using the HPA database to quantify its expression level and subcellular localization. CASC1 is abundantly expressed in tumor tissues, primarily in cytoplasmic vesicles and stroma. TIMER2 was used to analyze the correlation between CASC1 expression levels and the types of infiltrates associated with immune cells and immunosuppressive cells. MDSC, Treg, M2, and CAF were significantly correlated with CASC1 expression in various tumors. Comparing patients with and without CASC1 mutation, those with CASC1 mutation had worse overall survival, progression-free survival, and disease-free survival. The correlation between has-miR-150 and CASC1 (for the case of bladder cancer) was then analyzed, and the related ceRNA network was mapped. A negative relationship between CASC1 expression and has-miR-150 expression was found in cases of bladder cancer. And the presence of miR-150-targeted CASC1 may be associated with bladder cancer progression. CASC1 is expressed at elevated levels in various tumor tissues, and it is associated with tumorigenesis and development. Exosomes containing miR-150-targeted CASC1 may affect the progression of bladder cancer.
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Affiliation(s)
- Huarong Luo
- Department of Urology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China
| | - Chengdang Xu
- Department of Urology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China
| | - Bujun Ge
- Department of General Surgery, Tongji Hospital, Tongji University School of Medicine, Shanghai, China
| | - Tianru Wang
- Department of Urology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China
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Chen S, Li H, Li X, Chen W, Zhang X, Yang Z, Chen Z, Chen J, Zhang Y, Shi D, Song M. High SOX8 expression promotes tumor growth and predicts poor prognosis through GOLPH3 signaling in tongue squamous cell carcinoma. Cancer Med 2020; 9:4274-4289. [PMID: 32307911 PMCID: PMC7300415 DOI: 10.1002/cam4.3041] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/13/2019] [Revised: 02/24/2020] [Accepted: 03/14/2020] [Indexed: 01/29/2023] Open
Abstract
According to our previous study, GOLPH3 is markedly up-expressed in tongue squamous cell carcinoma (TSCC), which is also associated with poor survival. However, it remains unclear about key upstream and downstream mechanisms of GOLPH3. This study aimed to illuminate new mechanisms modulating GOLPH3 upregulation and promoting TSCC development at the molecular level. Using mass spectrometry and agarose-streptavidin-biotin pull-down analyses, SOX8 (SRY-Box 8) was identified to be the new protein to bind the GOLPH3 promoter within TSCC cells, which was further verified to be the regulator of GOLPH3 upregulation. The knockdown of SOX8 suppressed the promoter activity of GOLPH3, while secondarily inhibiting TSCC cell proliferation both in vivo and in vitro. Interestingly, GOLPH3 overexpression rescued the SOX8 knockdown-mediated suppression on TSCC proliferation. Additionally, exogenous over-expression of SOX8 also activated the activity of promoter as well as GOLPH3 expression, in the meantime of promoting TSCC development. Moreover it was discovered that SOX8 regulated GOLPH3 expression through interacting with TFAP2A. Moreover our results suggested that the SOX8 level was increased within tumor tissue compared with that in para-cancer normal counterpart, which showed positive correlation with the GOLPH3 level. According to Kaplan-Meier analyses, TSCC cases having higher SOX8 and GOLPH3 expression were associated with poorer prognostic outcomes. Taken together, this study reveals that SOX8 enhances the TSCC cell growth via the direct transcriptional activation of GOLPH3, which also indicates the potential to use SOX8/GOLPH3 pathway as the treatment target among TSCC patients.
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Affiliation(s)
- Shuwei Chen
- Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.,State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
| | - Huan Li
- State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.,Department of Intensive Care Unit, Sun Yat-sen University Cancer Center, Guangzhou, China
| | - Xiyuan Li
- Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.,State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
| | - Wenkuan Chen
- Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.,State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
| | - Xing Zhang
- Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.,State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
| | - Zhongyuan Yang
- Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.,State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
| | - Zhipeng Chen
- Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.,State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
| | - Jingtao Chen
- Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.,State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
| | - Ying Zhang
- Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.,State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
| | - Dingbo Shi
- State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.,Department of Experimental Research, Sun Yat-sen University Cancer Center, Guangzhou, China
| | - Ming Song
- Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.,State Key Laboratory of Oncology in South China, Guangzhou, China.,Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
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The Great Escape: how phosphatidylinositol 4-kinases and PI4P promote vesicle exit from the Golgi (and drive cancer). Biochem J 2019; 476:2321-2346. [DOI: 10.1042/bcj20180622] [Citation(s) in RCA: 34] [Impact Index Per Article: 5.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/16/2019] [Revised: 08/06/2019] [Accepted: 08/12/2019] [Indexed: 12/13/2022]
Abstract
Abstract
Phosphatidylinositol 4-phosphate (PI4P) is a membrane glycerophospholipid and a major regulator of the characteristic appearance of the Golgi complex as well as its vesicular trafficking, signalling and metabolic functions. Phosphatidylinositol 4-kinases, and in particular the PI4KIIIβ isoform, act in concert with PI4P to recruit macromolecular complexes to initiate the biogenesis of trafficking vesicles for several Golgi exit routes. Dysregulation of Golgi PI4P metabolism and the PI4P protein interactome features in many cancers and is often associated with tumour progression and a poor prognosis. Increased expression of PI4P-binding proteins, such as GOLPH3 or PITPNC1, induces a malignant secretory phenotype and the release of proteins that can remodel the extracellular matrix, promote angiogenesis and enhance cell motility. Aberrant Golgi PI4P metabolism can also result in the impaired post-translational modification of proteins required for focal adhesion formation and cell–matrix interactions, thereby potentiating the development of aggressive metastatic and invasive tumours. Altered expression of the Golgi-targeted PI 4-kinases, PI4KIIIβ, PI4KIIα and PI4KIIβ, or the PI4P phosphate Sac1, can also modulate oncogenic signalling through effects on TGN-endosomal trafficking. A Golgi trafficking role for a PIP 5-kinase has been recently described, which indicates that PI4P is not the only functionally important phosphoinositide at this subcellular location. This review charts new developments in our understanding of phosphatidylinositol 4-kinase function at the Golgi and how PI4P-dependent trafficking can be deregulated in malignant disease.
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Du FY, Zhou QF, Sun WJ, Chen GL. Targeting cancer stem cells in drug discovery: Current state and future perspectives. World J Stem Cells 2019; 11:398-420. [PMID: 31396368 PMCID: PMC6682504 DOI: 10.4252/wjsc.v11.i7.398] [Citation(s) in RCA: 64] [Impact Index Per Article: 10.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/20/2019] [Revised: 06/18/2019] [Accepted: 06/27/2019] [Indexed: 02/06/2023] Open
Abstract
In recent decades, cancer stem cells (CSCs) have been increasingly identified in many malignancies. CSC-related signaling pathways and their functions provide new strategies for treating cancer. The aberrant activation of related signaling pathways (e.g., Wnt, Notch, and Hedgehog pathways) has been linked to multiple types of malignant tumors, which makes these pathways attractive targets for cancer therapy. CSCs display many characteristic features, such as self-renewal, differentiation, high tumorigenicity, and drug resistance. Therefore, there is an urgent need to develop new therapeutic strategies to target these pathways to control stem cell replication, survival, and differentiation. Notable crosstalk occurs among different signaling pathways and potentially leads to compensatory escape. Therefore, multitarget inhibitors will be one of the main methods to overcome the drug resistance of CSCs. Many small molecule inhibitors of components of signaling pathways in CSCs have entered clinical trials, and some inhibitors, such as vismodegib, sonidegib, and glasdegib, have been approved. Tumor cells are susceptible to sonidegib and vismodegib resistance due to mutations in the Smo protein. The signal transducers and activators of transcription 3 (STAT3) inhibitor BBI608 is being evaluated in a phase III trial for a variety of cancers. Structural derivatives of BBI608 are the main focus of STAT3 inhibitor development, which is another strategy for CSC therapy. In addition to the potential pharmacological inhibitors targeting CSC-related signaling pathways, other methods of targeting CSCs are available, such as nano-drug delivery systems, mitochondrion targeting, autophagy, hyperthermia, immunotherapy, and CSC microenvironment targeting. In addition, we summarize the latest advances in the clinical development of agents targeting CSC-related signaling pathways and other methods of targeting CSCs.
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Affiliation(s)
- Fang-Yu Du
- Key Laboratory of Structure-Based Drug Design and Discovery of Ministry of Education, Shenyang Pharmaceutical University, Shenyang 110016, Liaoning Province, China
| | - Qi-Fan Zhou
- Key Laboratory of Structure-Based Drug Design and Discovery of Ministry of Education, Shenyang Pharmaceutical University, Shenyang 110016, Liaoning Province, China
| | - Wen-Jiao Sun
- Key Laboratory of Structure-Based Drug Design and Discovery of Ministry of Education, Shenyang Pharmaceutical University, Shenyang 110016, Liaoning Province, China
| | - Guo-Liang Chen
- Key Laboratory of Structure-Based Drug Design and Discovery of Ministry of Education, Shenyang Pharmaceutical University, Shenyang 110016, Liaoning Province, China
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Zheng YP, Zhang SB, Wang F, Liu H, Zhang W, Song B, Liu ZY, Xiong L, Fan YZ, Liao DY. Effects of lentiviral RNA interference-mediated downregulation of integrin-linked kinase on biological behaviors of human lens epithelial cells. Int J Ophthalmol 2016; 9:21-8. [PMID: 26949605 DOI: 10.18240/ijo.2016.01.04] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/08/2015] [Accepted: 06/09/2015] [Indexed: 11/23/2022] Open
Abstract
AIM To investigate the effects of lentivirus (LV) mediated integrin-linked kinase (ILK) RNA interference (RNAi) on biological behaviors of human lens epithelial cells (LECs). METHODS Human cataract LECs and immortalized human LEC line, human lens epithelial (HLE) B-3 cells were transfected by lentiviral vector expressing ILK-specific short hairpin RNA (shRNA) and then stimulated by transforming growth factor-β (TGF-β), the silencing of ILK gene and protein was identified by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot methods; biological behaviors including cell cycle and apoptosis, cell morphology, α-smooth muscle actin (SMA) stress fiber formation and cell migration were examined. RESULTS Remarkable decreases of ILK protein expression were detected in LECs carrying lentiviral ILK-shRNA vector; flow cytometry revealed arresting of cell cycle progression through the G1/S transition and higher apoptosis rate in ILK-RNAi-LV transfected cells. Less α-SMA stress fiber formation and migration was observed in ILK-RNAi-LV transfected LECs. CONCLUSION The present study demonstrated that ILK was an important regulator for LECs proliferation and migration. LV mediated ILK RNAi is an effective way to decrease ILK-regulated cell growth by arresting cell cycle progression and increasing cell apoptosis, as well as, to prevent cell migration by inhibiting TGF-β induced α-SMA stress fiber formation. Thus, LV mediated ILK RNAi might be useful to prevent posterior capsular opacification.
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Affiliation(s)
- Yu-Ping Zheng
- Department of Ophthalmology, the Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China
| | - Shao-Bo Zhang
- Department of Ophthalmology, Tangdu Hospital, the Fourth Military Medical University, Xi'an 710038, Shaanxi Province, China
| | - Feng Wang
- Department of Ophthalmology, the Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China
| | - Hui Liu
- Department of Otolaryngology, Shaanxi Provincial People's Hospital, Xi'an 710068, Shaanxi Province, China
| | - Wen Zhang
- Department of Otolaryngology, Shaanxi Provincial People's Hospital, Xi'an 710068, Shaanxi Province, China
| | - Bin Song
- Department of Otolaryngology, Shaanxi Provincial People's Hospital, Xi'an 710068, Shaanxi Province, China
| | - Zi-Yao Liu
- Department of Ophthalmology, the Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China
| | - Lei Xiong
- Department of Ophthalmology, the Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China
| | - Ya-Zhi Fan
- Department of Ophthalmology, the Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China
| | - Ding-Ying Liao
- Department of Ophthalmology, the Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China
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Zhang Q, Zhuang J, Deng Y, Zhao X, Tang B, Yao D, Zhao W, Chang C, Lu Q, Chen W, Zhang S, Ji C, Cao L, Guo H. GOLPH3 is a potential therapeutic target and a prognostic indicator of poor survival in bladder cancer treated by cystectomy. Oncotarget 2015; 6:32177-32192. [PMID: 26375441 PMCID: PMC4741668 DOI: 10.18632/oncotarget.4867] [Citation(s) in RCA: 21] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/16/2015] [Accepted: 08/12/2015] [Indexed: 11/28/2022] Open
Abstract
Golgi phosphoprotein 3 (GOLPH3) has been reported to be involved in the development of several human cancers. However, its clinical significance and biological role in bladder cancer remains unclear. In this study, we sought to analyze the GOLPH3 expression in bladder cancer samples and cells, and explore its clinical significance and biological role. We found that GOLPH3 was significantly increased in bladder cancer tissues and cells. Overexpression of GOLPH3 had significant correlation with poorer survival for bladder cancer patients treated by cystectomy. Knockdown of GOLPH3 inhibited the proliferation, migration and invasion of cancer cells, and tumor growth in a xenograft mouse model. GOLPH3 silencing inhibited AKT/m-TOR signaling, increased the cyclin-dependent kinase (CDK) inhibitor p27 and decreased the CDK regulator cyclin D1 and matrix metallopeptidase 9 (MMP9). Thus, GOLPH3 is likely to play important roles in bladder cancer progression via modulating AKT/mTOR signaling, and it is a novel prognostic biomarker and promising therapeutic target for bladder cancer.
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Affiliation(s)
- Qing Zhang
- Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing 210008, Jiangsu, PR China
| | - Junlong Zhuang
- Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing 210008, Jiangsu, PR China
| | - Yongming Deng
- Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing 210008, Jiangsu, PR China
| | - Xiaozhi Zhao
- Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing 210008, Jiangsu, PR China
| | - Bo Tang
- Vazyme Biotech Co., Ltd, Nanjing 210000, Jiangsu, PR China
| | - Dongwei Yao
- Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing 210008, Jiangsu, PR China
| | - Wei Zhao
- MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing, Jiangsu 210061, China
| | - Cunjie Chang
- MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing, Jiangsu 210061, China
| | - Qun Lu
- Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing 210008, Jiangsu, PR China
| | - Wei Chen
- Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing 210008, Jiangsu, PR China
| | - Shiwei Zhang
- Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing 210008, Jiangsu, PR China
| | - Changwei Ji
- Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing 210008, Jiangsu, PR China
| | - Lin Cao
- College of Food Science and Technology, Nanjing Agricultural University, Nanjing 210095, Jiangsu, PR China
- Vazyme Biotech Co., Ltd, Nanjing 210000, Jiangsu, PR China
| | - Hongqian Guo
- Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing 210008, Jiangsu, PR China
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Lu M, Tian Y, Yue WM, Li L, Li SH, Qi L, Hu WS, Gao C, Si LB, Tian H. GOLPH3, a good prognostic indicator in early-stage NSCLC related to tumor angiogenesis. Asian Pac J Cancer Prev 2015; 15:5793-8. [PMID: 25081702 DOI: 10.7314/apjcp.2014.15.14.5793] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/10/2022] Open
Abstract
BACKGROUND Golgi phosphoprotein-3 (GOLPH3) is implicated in cancer development and progression. The aim of this study was to evaluate the prognostic significance of GOLPH3 protein and its association with tumor angiogenesis in patients with early-stage NSCLC. MATERIALS AND METHODS Immunohistochemistry was performed to determine GOLPH3 protein expression and allow assessment of intratumoral microvessel density (MVD) by counting CD-34 positive immunostained endothelial cells. Correlations of expression with MVD, clinicopathologic features and clinical prognosis were analyzed. RESULTS A notably higher level of GOLPH3 expression was found in early-stage NSCC tissues at the protein level. However, we do not find any correlation between GOLPH3 expression and clinicopathologic features (p>0.05), although higher MVD was positively associated with GOLPH3 overexpression (p<0.001). Expression of GOLPH3 was found to be an independent prognostic factor in early- stage NSCLC patients, those expressing high levels of GOLPH3 exhibiting a substantially lower 5-year overall survival than GOLPH3-negative patients (adjusted HR =1.899, 95% CI: 1.021-3.532, p=0.043). CONCLUSIONS High expression of the GOLPH3 protein is common in early-stage NSCC, and is closely associated with tumor progression, increased tumor angiogenesis, and poor survival. We conclude a possibility of its use as a diagnostic and prognostic marker in early-stage NSCC patients.
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Affiliation(s)
- Ming Lu
- Department of Thoracic Surgery, Qilu Hospital, Shandong University, Jinan, China E-mail :
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Li H, Zhou F, Wang H, Lin D, Chen G, Zuo X, Sun L, Zhang X, Yang S. Knockdown of EIF3D suppresses proliferation of human melanoma cells through G2/M phase arrest. Biotechnol Appl Biochem 2015; 62:615-20. [PMID: 25322666 DOI: 10.1002/bab.1305] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/01/2014] [Accepted: 10/10/2014] [Indexed: 12/18/2022]
Affiliation(s)
- Hui Li
- Department of Dermatology; Institute of Dermatology; The First Affiliated Hospital; Anhui Medical University; Hefei Anhui People's Republic of China
| | - Fusheng Zhou
- Department of Dermatology; Institute of Dermatology; The First Affiliated Hospital; Anhui Medical University; Hefei Anhui People's Republic of China
| | - Hongyan Wang
- Department of Dermatology; Institute of Dermatology; The First Affiliated Hospital; Anhui Medical University; Hefei Anhui People's Republic of China
| | - Da Lin
- Department of Dermatology; Institute of Dermatology; The First Affiliated Hospital; Anhui Medical University; Hefei Anhui People's Republic of China
| | - Gang Chen
- Department of Dermatology; Institute of Dermatology; The First Affiliated Hospital; Anhui Medical University; Hefei Anhui People's Republic of China
| | - Xianbo Zuo
- Department of Dermatology; Institute of Dermatology; The First Affiliated Hospital; Anhui Medical University; Hefei Anhui People's Republic of China
| | - Liangdan Sun
- Department of Dermatology; Institute of Dermatology; The First Affiliated Hospital; Anhui Medical University; Hefei Anhui People's Republic of China
| | - Xuejun Zhang
- Department of Dermatology; Institute of Dermatology; The First Affiliated Hospital; Anhui Medical University; Hefei Anhui People's Republic of China
| | - Sen Yang
- Department of Dermatology; Institute of Dermatology; The First Affiliated Hospital; Anhui Medical University; Hefei Anhui People's Republic of China
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Li Y, Gao Y, Xu Y, Sun X, Song X, Ma H, Yang M. si-RNA-mediated knockdown of PDLIM5 suppresses gastric cancer cell proliferation in vitro. Chem Biol Drug Des 2014; 85:447-53. [PMID: 25215606 DOI: 10.1111/cbdd.12428] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/17/2014] [Revised: 08/20/2014] [Accepted: 08/27/2014] [Indexed: 12/14/2022]
Abstract
Gastric cancer is the second most prominent cause of cancer mortality in the world. This study was designed to identify the possible use of si-RNA-mediated PDLIM5 gene silencing as a therapeutic tool for gastric cancer. Expression levels of PDLIM5 were detected in several gastric cancer cell lines using Western blot and qRT-PCR. We found PDLIM5 is highly expressed in all cultured gastric cancer cell lines. Small interfering RNA (si-RNA) was then employed to knock down PDLIM5 expression in MGC80-3 gastric cancer cells. Knockdown of PDLIM5 significantly inhibited cell proliferation and colony formation. Moreover, the absence of PDLIM5 in MGC80-3 cells led to S phase cell cycle arrest and apoptosis. This study highlights the critical role of PDLIM5 in gastric cancer cell growth and suggests that si-RNA-mediated silencing of PDLIM5 might serve as a potential therapeutic approach for the treatment of gastric cancer.
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Affiliation(s)
- Yanliang Li
- Department of Gastrointestinal Surgery, Shandong Tumor Hospital, Jinan, 250117, China
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