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Zhao Y, Wu S, Cao G, Song P, Lan CG, Zhang L, Sang YH. Mitochondrial carrier homolog 2 is important for mitochondrial functionality and non-small cell lung cancer cell growth. Cell Death Dis 2025; 16:95. [PMID: 39948081 PMCID: PMC11825924 DOI: 10.1038/s41419-025-07419-0] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/12/2024] [Revised: 01/13/2025] [Accepted: 02/03/2025] [Indexed: 02/16/2025]
Abstract
Discovering new molecular targets for non-small cell lung cancer (NSCLC) is critically important. Enhanced mitochondrial function can promote NSCLC progression by enabling metabolic reprogramming, resistance to apoptosis, and increased cell proliferation. Mitochondrial carrier homolog 2 (MTCH2), located in the outer mitochondrial membrane, is pivotal in regulating mitochondrial activities. This study examines MTCH2 expression and its functional role in NSCLC. Bioinformatic analysis showed that MTCH2 is overexpressed in NSCLC tissues, correlating with poor prognosis and other key clinical parameters of the patients. In addition, single-cell sequencing data revealed higher MTCH2 expression levels in cancer cells of NSCLC tumor mass. Moreover, MTCH2 is also upregulated in locally-treated NSCLC tissues and multiple primary/established human NSCLC cells. In various NSCLC cells, silencing MTCH2 via targeted shRNA or knockout (KO) using the CRISPR/Cas9 method significantly hindered cell proliferation, migration and invasion, while inducing apoptosis. MTCH2 knockdown or KO robustly impaired mitochondrial function, as indicated by reduced mitochondrial respiration, decreased complex I activity, lower ATP levels, lower mitochondrial membrane potential (mitochondrial depolarization), and increased reactive oxygen species (ROS) production. Conversely, ectopic overexpression of MTCH2 in primary NSCLC cells enhanced mitochondrial complex I activity and ATP production, promoting cell proliferation and migration. In vivo, the intratumoral injection of MTCH2 shRNA adeno-associated virus (aav) impeded the growth of subcutaneous xenografts of primary NSCLC cells in nude mice. In MTCH2 shRNA aav-injected NSCLC xenograft tissues, there was decreases in MTCH2 expression, mitochondrial complex I activity, ATP content, and the glutathione (GSH)/glutathione disulfide (GSSG) ratio, but increase in thiobarbituric acid reactive substances (TBAR) activity. Additionally, MTCH2 silencing led to reduced Ki-67 staining but increased apoptosis in NSCLC xenografts. Collectively, these findings demonstrate that overexpressed MTCH2 promotes NSCLC cell growth potentially through the maintenance of mitochondrial hyper-function, highlighting MTCH2 as a novel and promising therapeutic target for treating this disease.
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Affiliation(s)
- Yong Zhao
- Department of Thoracic Surgery, Affiliated Hospital of Jiangnan University, Wuxi, China
| | - Siyang Wu
- Respiratory Intensive Care Unit, Affiliated Hospital of YouJiang Medical University for Nationalities, Baise, China
| | - Guohong Cao
- Department of Respiratory and Critical Care Medicine, Binzhou Medical University Hospital, Binzhou Medical University, Binzhou, China
| | - Peidong Song
- Department of Cardiothoracic Surgery, the Second Affiliated Hospital of Soochow University, Suzhou, China
| | - Chang-Gong Lan
- Guangxi Key Laboratory of basic and translational research of Bone and Joint Degenerative Diseases, Guangxi Biomedical Materials Engineering Research Center for Bone and Joint Degenerative Diseases, Baise, China.
- Department of Orthopaedics, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China.
| | - Lin Zhang
- Department of Thoracic Surgery, Suzhou Ninth People's Hospital Affiliated to Soochow University, Suzhou, China.
| | - Yong-Hua Sang
- Department of Cardiothoracic Surgery, the Second Affiliated Hospital of Soochow University, Suzhou, China.
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Zhang L, Wang J, Deng W, Gui F, Peng F, Zhu Q. Solamargine Induces Hepatocellular Carcinoma Cell Apoptosis and Ferroptosis via Regulating STAT1/MTCH1 Axis. Biochem Genet 2025; 63:210-224. [PMID: 38429602 DOI: 10.1007/s10528-024-10749-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/22/2023] [Accepted: 02/17/2024] [Indexed: 03/03/2024]
Abstract
BACKGROUND Solamargine (SM) has been shown to play anti-tumor role in hepatocellular carcinoma (HCC). However, the underlying molecular mechanisms of SM in HCC progression deserve further exploration. METHODS HCC cell proliferation and apoptosis were assessed by cell counting kit 8 assay, colony formation assay and flow cytometry. Ferroptosis was evaluated by detecting the levels of Fe2+, iron, MDA, ROS and GSH in HCC cells. In addition, mitochondrial carrier 1 (MTCH1) mRNA level was detected by quantitative real-time PCR. Western blot was used to test MTCH1 and signal transduction and activation of transcription 1 (STAT1) protein levels. Dual-luciferase reporter assay was employed to analyze the interaction between STAT1 and MTCH1. A mouse xenograft model was also constructed to explore the role of SM in vivo. RESULTS SM could potentially suppress HCC cell growth by inducing ferroptosis. MTCH1 was highly expressed in HCC tissues and cells, and its silencing inhibited HCC cell proliferation, promoted apoptosis and ferroptosis. MTCH1 expression was reduced by SM, and its overexpression reversed SM-induced HCC cell apoptosis and ferroptosis. Furthermore, STAT1 facilitated MTCH1 transcription and promoted its expression. Besides, STAT1 expression could be reduced by SM, and its overexpression abolished the decreasing effect of SM on MTCH1 expression. In vivo, SM suppressed HCC tumor growth by reducing MTCH1 expression. CONCLUSION SM promoted HCC cell apoptosis and ferroptosis via the STAT1/MTCH1 axis.
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Affiliation(s)
- Limei Zhang
- Department of Gastroenterology, Shenzhen Longhua District Central Hospital, No.187, Guanlan Street, Shenzhen, 518110, China
| | - Jinfu Wang
- Department of Gastroenterology, Shenzhen Longhua District Central Hospital, No.187, Guanlan Street, Shenzhen, 518110, China
| | - Weiping Deng
- Department of Gastroenterology, Shenzhen Longhua District Central Hospital, No.187, Guanlan Street, Shenzhen, 518110, China
| | - Fenfang Gui
- Department of Gastroenterology, Shenzhen Longhua District Central Hospital, No.187, Guanlan Street, Shenzhen, 518110, China
| | - Fanzhou Peng
- Department of Gastroenterology, Shenzhen Longhua District Central Hospital, No.187, Guanlan Street, Shenzhen, 518110, China
| | - Qian Zhu
- Department of Gastroenterology, Shenzhen Longhua District Central Hospital, No.187, Guanlan Street, Shenzhen, 518110, China.
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Yan Y, Cao L, Gu L, Xu C, Lu J, Lv D, Tian J, Yin X, Pu J, Zhang B, Zhao G. Analysis of Common Genetic Variation of Anxiety Disorders in Essential Tremor. J Mol Neurosci 2025; 75:14. [PMID: 39890685 DOI: 10.1007/s12031-024-02226-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/27/2024] [Accepted: 04/15/2024] [Indexed: 02/03/2025]
Abstract
The objective of this study is to explore the association of common genetic variation of anxiety disorders and essential tremor (ET). We genotyped 25 anxiety-specific risk variants in a cohort of 478 unrelated ET patients and 504 age and gender-matched healthy controls from eastern China using a MassARRAY system. The association between candidate variants and ET patients was evaluated using gene-based analysis. A total of 159 patients (33.3%) had anxiety. In genotypic analysis, rs708012 (in an intergenic region) in the dominant models was found to be significantly associated with ET (P < 0.001, OR = 0.605). In allelic analysis, the carriers of the C allele of NTRK2 rs1187280 (P = 0.027, OR = 0.626), T allele of TMEM106B rs3807866 (P = 0.030, OR = 1.287), and T allele of rs708012 (P < 0.001, OR = 0.679) occupy a larger proportion of ET patients compared with healthy controls. Anxiety-specific risk SNPs of TMEM106B rs3807866 increase the risk for ET, while two SNPs of NTRK2 rs1187280 and rs708012 show a protective role.
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Affiliation(s)
- Yaping Yan
- Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No. 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China
| | - Lanxiao Cao
- Department of Neurology, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, N1 Shangcheng Avenue, Yiwu, 322000, Zhejiang, China
| | - Luyan Gu
- Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No. 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China
| | - Congying Xu
- Department of Neurology, Jiaxing Second Hospital, Jiaxing, China
| | - Jinyu Lu
- Department of Neurology, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, N1 Shangcheng Avenue, Yiwu, 322000, Zhejiang, China
| | - Dayao Lv
- Department of Neurology, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, N1 Shangcheng Avenue, Yiwu, 322000, Zhejiang, China
| | - Jun Tian
- Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No. 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China
| | - Xinzhen Yin
- Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No. 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China
| | - Jiali Pu
- Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No. 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China
| | - Baorong Zhang
- Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No. 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China.
| | - Guohua Zhao
- Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No. 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China.
- Department of Neurology, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, N1 Shangcheng Avenue, Yiwu, 322000, Zhejiang, China.
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Wang L, Gong WH. Predictive model using four ferroptosis-related genes accurately predicts gastric cancer prognosis. World J Gastrointest Oncol 2024; 16:2018-2037. [PMID: 38764813 PMCID: PMC11099433 DOI: 10.4251/wjgo.v16.i5.2018] [Citation(s) in RCA: 3] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/21/2023] [Revised: 01/31/2024] [Accepted: 03/08/2024] [Indexed: 05/09/2024] Open
Abstract
BACKGROUND Gastric cancer (GC) is a common malignancy of the digestive system. According to global 2018 cancer data, GC has the fifth-highest incidence and the third-highest fatality rate among malignant tumors. More than 60% of GC are linked to infection with Helicobacter pylori (H. pylori), a gram-negative, active, microaerophilic, and helical bacterium. This parasite induces GC by producing toxic factors, such as cytotoxin-related gene A, vacuolar cytotoxin A, and outer membrane proteins. Ferroptosis, or iron-dependent programmed cell death, has been linked to GC, although there has been little research on the link between H. pylori infection-related GC and ferroptosis. AIM To identify coregulated differentially expressed genes among ferroptosis-related genes (FRGs) in GC patients and develop a ferroptosis-related prognostic model with discrimination ability. METHODS Gene expression profiles of GC patients and those with H. pylori-associated GC were obtained from The Cancer Genome Atlas and Gene Expression Omnibus (GEO) databases. The FRGs were acquired from the FerrDb database. A ferroptosis-related gene prognostic index (FRGPI) was created using least absolute shrinkage and selection operator-Cox regression. The predictive ability of the FRGPI was validated in the GEO cohort. Finally, we verified the expression of the hub genes and the activity of the ferroptosis inducer FIN56 in GC cell lines and tissues. RESULTS Four hub genes were identified (NOX4, MTCH1, GABARAPL2, and SLC2A3) and shown to accurately predict GC and H. pylori-associated GC. The FRGPI based on the hub genes could independently predict GC patient survival; GC patients in the high-risk group had considerably worse overall survival than did those in the low-risk group. The FRGPI was a significant predictor of GC prognosis and was strongly correlated with disease progression. Moreover, the gene expression levels of common immune checkpoint proteins dramatically increased in the high-risk subgroup of the FRGPI cohort. The hub genes were also confirmed to be highly overexpressed in GC cell lines and tissues and were found to be primarily localized at the cell membrane. The ferroptosis inducer FIN56 inhibited GC cell proliferation in a dose-dependent manner. CONCLUSION In this study, we developed a predictive model based on four FRGs that can accurately predict the prognosis of GC patients and the efficacy of immunotherapy in this population.
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Affiliation(s)
- Li Wang
- Department of Emergency, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310000, Zhejiang Province, China
| | - Wei-Hua Gong
- Department of Surgery, The Second Affiliated Hospital Zhejiang University School of Medicine, Hangzhou 310052, Zhejiang Province, China
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Zhang JW, Huang LY, Li YN, Tian Y, Yu J, Wang XF. Mitochondrial carrier homolog 2 increases malignant phenotype of human gastric epithelial cells and promotes proliferation, invasion, and migration of gastric cancer cells. World J Gastrointest Oncol 2024; 16:991-1005. [PMID: 38577443 PMCID: PMC10989370 DOI: 10.4251/wjgo.v16.i3.991] [Citation(s) in RCA: 1] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/20/2023] [Revised: 12/21/2023] [Accepted: 01/19/2024] [Indexed: 03/12/2024] Open
Abstract
BACKGROUND The precise role of mitochondrial carrier homolog 2 (MTCH2) in promoting malignancy in gastric mucosal cells and its involvement in gastric cancer cell metastasis have not been fully elucidated. AIM To determine the role of MTCH2 in gastric cancer. METHODS We collected 65 samples of poorly differentiated gastric cancer tissue and adjacent tissues, constructed MTCH2-overexpressing and MTCH2-knockdown cell models, and evaluated the proliferation, migration, and invasion of human gastric epithelial cells (GES-1) and human gastric cancer cells (AGS) cells. The mitochondrial membrane potential (MMP), mitochondrial permeability transformation pore (mPTP) and ATP fluorescence probe were used to detect mitochondrial function. Mitochondrial function and ATP synthase protein levels were detected via Western blotting. RESULTS The expression of MTCH2 and ATP2A2 in gastric cancer tissues was significantly greater than that in adjacent tissues. Overexpression of MTCH2 promoted colony formation, invasion, migration, MMP expression and ATP production in GES-1 and AGS cells while upregulating ATP2A2 expression and inhibiting cell apoptosis; knockdown of MTCH2 had the opposite effect, promoting overactivation of the mPTP and promoting apoptosis. CONCLUSION MTCH2 can increase the malignant phenotype of GES-1 cells and promote the proliferation, invasion, and migration of gastric cancer cells by regulating mitochondrial function, providing a basis for targeted therapy for gastric cancer cells.
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Affiliation(s)
- Jing-Wen Zhang
- School of Basic Medical Science, NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
| | - Ling-Yan Huang
- Department of Pathology, General Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
| | - Ya-Ning Li
- School of Basic Medical Science, NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
| | - Ying Tian
- School of Clinical Medicine, Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
| | - Jia Yu
- School of Basic Medical Science, NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
| | - Xiao-Fei Wang
- Department of Pathology, North China University of Science and Technology Affiliated Hospital, Tangshan 063000, Hebei Province, China
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Wang X, Ji Y, Qi J, Zhou S, Wan S, Fan C, Gu Z, An P, Luo Y, Luo J. Mitochondrial carrier 1 (MTCH1) governs ferroptosis by triggering the FoxO1-GPX4 axis-mediated retrograde signaling in cervical cancer cells. Cell Death Dis 2023; 14:508. [PMID: 37550282 PMCID: PMC10406804 DOI: 10.1038/s41419-023-06033-2] [Citation(s) in RCA: 10] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/21/2023] [Revised: 07/17/2023] [Accepted: 08/01/2023] [Indexed: 08/09/2023]
Abstract
Cervical cancer is one of the leading causes of cancer death in women. Mitochondrial-mediated ferroptosis (MMF) is a recently discovered form of cancer cell death. However, the role and the underlying mechanism of MMF in cervical cancer remain elusive. Here, using an unbiased screening for mitochondrial transmembrane candidates, we identified mitochondrial carrier 1 (MTCH1) as a central mediator of MMF in cervical cancers. MTCH1-deficiency disrupted mitochondrial oxidative phosphorylation while elevated mitochondrial reactive oxygen species (ROS) by decreasing NAD+ levels. This mitochondrial autonomous event initiated a mitochondria-to-nucleus retrograde signaling involving reduced FoxO1 nuclear translocation and subsequently downregulation of the transcription and activity of a key anti-ferroptosis enzyme glutathione peroxidase 4 (GPX4), thereby elevating ROS and ultimately triggering ferroptosis. Strikingly, targeting MTCH1 in combination with Sorafenib effectively and synergistically inhibited the growth of cervical cancer in a nude mouse xenograft model by actively inducing ferroptosis. In conclusion, these findings enriched our understanding of the mechanisms of MMF in which MTCH1 governed ferroptosis though retrograde signaling to FoxO1-GPX4 axis, and provided a potential therapeutic target for treating cervical cancer.
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Affiliation(s)
- Xuan Wang
- Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, 100193, Beijing, China
| | - Yuting Ji
- Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, 100193, Beijing, China
- Greater Bay Area Institute of Precision Medicine (Guangzhou), Fudan University, Nansha District, 511400, Guangzhou, China
- Institute of Life Sciences, Fudan University, 200433, Shanghai, China
| | - Jingyi Qi
- Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, 100193, Beijing, China
| | - Shuaishuai Zhou
- Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, 100193, Beijing, China
| | - Sitong Wan
- Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, 100193, Beijing, China
| | - Chang Fan
- Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, 100193, Beijing, China
| | - Zhenglong Gu
- Greater Bay Area Institute of Precision Medicine (Guangzhou), Fudan University, Nansha District, 511400, Guangzhou, China
- Institute of Life Sciences, Fudan University, 200433, Shanghai, China
| | - Peng An
- Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, 100193, Beijing, China.
| | - Yongting Luo
- Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, 100193, Beijing, China.
| | - Junjie Luo
- Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, 100193, Beijing, China.
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Chen L, Lin Y, Liu G, Xu R, Hu Y, Xie J, Yu H. Clinical Value for Diagnosis and Prognosis of Signal Sequence Receptor 1 (SSR1) and Its Potential Mechanism in Hepatocellular Carcinoma: A Comprehensive Study Based on High-Throughput Data Analysis. Int J Gen Med 2021; 14:7435-7451. [PMID: 34744454 PMCID: PMC8566009 DOI: 10.2147/ijgm.s336725] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/30/2021] [Accepted: 10/20/2021] [Indexed: 12/19/2022] Open
Abstract
Objective Hepatocellular Carcinoma (HCC) has the characteristics of high incidence and poor prognosis. However, the underlying mechanism of HCC has not yet been fully elucidated. This study aims to investigate the potential mechanism and clinical significance of signal sequence receptor (SSR1) in HCC through bioinformatics methods. Methods Four online (GEPIA, TIMER, TCGA, and GEO) databases were used to explore the expression level of SSR1 in HCC. The summary receiver operating characteristic (SROC) analysis and standardized mean difference (SMD) calculation were performed further to detect its diagnostic ability and expression level. The Human Protein Atlas (HPA) database was applied to verify the level of SSR1 protein expression. Chi-square test and Fisher’s exact test were carried out to determine the clinical relevance of SSR1 expression. KM survival analysis, univariate and multivariate COX regression analyses were employed to explore the prognostic impact of SSR1. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and Gene set enrichment analysis (GSEA) were implemented to reveal the underlying mechanism of SSR1. Quantitative Real-Time Polymerase Chain Reaction (QRT-PCR) was used to verify the expression of SSR1 in HCC. Results SSR1 was significantly overexpressed in HCC (SMD=1.25, P=0.03) and had the moderate diagnostic ability (AUC=0.84). SSR1 expression was significantly correlated with T stage, Gender, Pathologic stage (All P<0.05). Patients with high SSR1 expression had shorter overall survival (OS). Univariate and multivariate Cox regression analyses showed that high SSR1 expression was an independent risk factor for poor prognosis. KEGG analysis showed that SSR1-related genes were enriched in the cell cycle, DNA replication, and TGF-beta signaling pathway. GSEA analysis also shows that the high expression of SSR1 is related to the activation of the above three signal pathways. qRT-PCR showed that the SSR1 expression in HCC was significantly higher than the Peri-carcinoma tissue (PHCC) and the corresponding normal liver tissue. Conclusion SSR1 expression was significantly up-regulated, and it had the potential as a biomarker for the diagnosis and prognosis of HCC. It was very likely to participate in the occurrence and development of HCC by regulating the cell cycle. In summary, our study comprehensively analyzed the clinical value of SSR1 and also conducted a preliminary study on its potential mechanism, which will provide inspiration for the in-depth study of SSR1 in HCC.
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Affiliation(s)
- Liang Chen
- Department of General Surgery, Fuyang Hospital Affiliated to Anhui Medical University, Fuyang, Anhui, People's Republic of China
| | - Yunhua Lin
- The First Clinical Medical College, Guangxi Medical University, Nanning, Guangxi, People's Republic of China
| | - Guoqing Liu
- The First Clinical Medical College, Guangxi Medical University, Nanning, Guangxi, People's Republic of China
| | - Rubin Xu
- Department of General Surgery, Fuyang Hospital Affiliated to Anhui Medical University, Fuyang, Anhui, People's Republic of China
| | - Yiming Hu
- College of Pharmacy, Jiangsu Ocean University, Lianyungang, Jiangsu, People's Republic of China
| | - Jiaheng Xie
- Department of Burn and Plastic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, People's Republic of China
| | - Hongzhu Yu
- Department of General Surgery, Fuyang Hospital Affiliated to Anhui Medical University, Fuyang, Anhui, People's Republic of China
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