Zhi‐Xiang Zhou

University of South China

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Huiting Liu

Affiliated Hospital of Youjiang Medical University for Nationalities

Zhong Ren

Hunan University of Traditional Chinese Medicine

Nian-Hua Deng

University of South China

Kun Zhou

Boston Children's Hospital

Jianwei Liang

Chinese Academy of Medical Sciences & Peking Union Medical College

Zhen Tian

Heilongjiang Institute of Technology

Zhi‐Sheng Jiang

University of South China

Yongqian Jiang

Yancheng First People's Hospital

Wenhao Xiong

Guizhou University

Xiaofeng Ma

University of South China

Cooperative Institutions

University of South China

Chinese Academy of Medical Sciences & Peking Union Medical College

Sun Yat-sen University

Peking Union Medical College Hospital

Sun Yat-sen University Cancer Center

Wenzhou Medical University

Sichuan University

Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University

State Key Laboratory of Oncology in South China

Peking University

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LncRNA-mediated Modulation of Endothelial Cells: Novel Progress in the Pathogenesis of Coronary Atherosclerotic Disease

Current Medicinal Chemistry (2023)

Shao Ouyang Zhi‐Xiang Zhou Huiting Liu Zhong Ren Huan Liu

Coronary atherosclerotic disease (CAD) is a common cardiovascular disease and an important cause of death. Moreover, endothelial cells (ECs) injury is an early pathophysiological feature of CAD, and long noncoding RNAs (lncRNAs) can modulate gene expression. Recent studies have shown that lncRNAs are involved in the pathogenesis of CAD, especially by regulating ECs. In this review, we summarize the novel progress of lncRNA-modulated ECs in the pathogenesis of CAD, including ECs proliferation, migration, adhesion, angiogenesis, inflammation, apoptosis, autophagy, and pyroptosis. Thus, as lncRNAs regulate ECs in CAD, lncRNAs will provide ideal and novel targets for the diagnosis and drug therapy of CAD.

Pathogenesis

Pyroptosis

10.2174/0929867330666230213100732

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Clinical observation of airway pressure release ventilation in moderate and severe acute respiratory distress syndrome

Chin J Lung Dis(Electronic Edition) (2017)

Zhi‐Xiang Zhou

Objective To explore the clinical effects of airway pressure release ventilation, (APRV) in moderate and severe acute respiratory distress syndrome(ARDS). Methods All 60 patients with moderate and severe ARDS from June 2013 to June 2016 in The Second People′s Hospital of Hainan Province were researched. They were divided into two groups by randomly, APRV group and tidal volume lung protection ventilation group, using volume synchronous intermittent mandatory ventilation and positive end expiratory pressure(SIMV group), each of 30 cases. The ventilation effect of two groups were compared. Results After ventilation 1 d, 2 d, 3 d, the peak airway pressure (Ppeak), mean airway pressure (Pmean), oxygenation index (PaO2/FiO2), extravascular lung water index (ELWI), heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ), Murray acute lung injury score of two groups were improved before ventilation(P 0.05), there was no significant difference in mortality rate between the two groups in 1 months(P>0.05). Conclusion It is improved that the effective respiratory support in patients with moderate to severe ARDS using APRV ventilation, it′s worthy of application and promotion. Key words: Acute respiratory distress syndrome; Moderate and severe; Airway pressure release ventilation; Tidal volume lung protective ventilation

Mean airway pressure

Peak inspiratory pressure

Respiratory Rate

10.3877/cma.j.issn.1674-6902.2017.04.013

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[Application of sigmoid coloplasty in super-lower anastomosis].

PubMed (2005)

Zhi‐Xiang Zhou Yongfu Shao Ping Zhao Xiaofeng Bai Bing Wang

To assess the clinical value of sigmoid coloplasty of super-lower anastomosis.Thirty-five patients underwent sigmoid coloplasty (treatment group), while 33 patients received straight sigmoidorectostomy (control group). Complication rate and anal function were observed and compared between the two groups.The complication rate was 17.1% and 21.2% in the study group and control group respectively (P> 0.05). Average stool frequency were 2 times (1-5.5 times) a day in the study group and 3.5 times (1-9 times) a day in the control group 12 months after operation (P< 0.01). The fecal continence and self-satisfaction were improved significantly in the study group than that of the control group(P< 0.01, respectively). The postoperative anal function score was 2.57 in the study group and 7.21 in the control group, there was significant difference between the two groups (P< 0.01).Compared with straight sigmoidorectostomy, sigmoid coloplasty applied in super-lower anastomosis can significantly improve the recovery of anal function without increasing complication rates.

Sigmoid function

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The Magic and Mystery of TRIM65 in Diseases

Current Medicinal Chemistry (2024)

Qinyi Zhou Yuan Li Zhi‐Xiang Zhou Yiren Zhou Yizhou Liu

Abstract: Tripartite-motif protein family member 65 (TRIM65) belongs to the tripartite motif (TRIM) protein family. Its typical structure consists of the RING, B-Box motif, and coiled-coil domains, which are highly conserved at the N-terminus and the variable SPRY domain at the C-terminus. TRIM65 is an E3 ubiquitin ligase that participates in physiological and pathological processes through the ubiquitination pathway, including intracellular signal transduction, protein degradation, cell proliferation, apoptosis, carcinogenesis, autophagy, and phenotypic transformation. Evidence shows that TRIM65 plays a remarkable and obscure role in diseases, including multisystem tumours, neurodegenerative diseases, immune system diseases, and inflammatory diseases. This review is devoted to elaborating on the relationship between TRIM65 and diseases and its pathogenic mechanism, providing a theoretical basis for TRIM65 as a possible pathogenic target of diseases and exploring the possible future research direction of TRIM65 and the challenges it may face.

Ubiquitin-Protein Ligases

Protein family

10.2174/0109298673304966240614091547

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HPV18 E6 and E7 Intratumour Heterogeneity in Esophageal Cancer

Journal of Cancer Therapy (2019)

Sara Khodahemmati Maliha Gaffar Jintao Li Yangjunqi Wang Xiaoli Wang

The development of esophageal cancer accompanied by the presence of human papillomavirus (HPV) DNA into the host genome. By evaluating the expression of this virus for tumor cell origin and also their cell grows and migrations, we examined esophageal cancer clonality in the context of intra-tumor heterogeneity. In this research, we have checked the expression of HPV18 E6 and E7 in different single cell clones by the manual cell picking method in the HPV positive esophageal cancer (EC109), EC109 cell line used as a negative control, and Hela cell line used as the positive control. Quantitative real-time PCR (QRT-PCR) was run to detect the expression levels of HPV E6 and E7, Cell Counting Kit-8 (CCK-8) assay was used to examine cell proliferation, invasion assays performed using Costar chambers and wounding assay to study cell migrations in vitro. We investigated the intra-tumor heterogeneity of HPV E6 and E7 in esophageal cancer and the evaluation of the growth and migrations at the clonal level, using 10 single cell clones. In particular clones, C7 & C10 displayed a highly variable expression in both HPV E6 and E7 and weak in four clones (C1, C3, C4, and C9) consequently, the cell invasion, proliferation, and migration increase with increasing the level of HPV expression and inverse. In conclusion, the resulting based on single cell cloning showed the relationship between HPV and cell growth and migration in esophageal cancer. Future study in HPV DNA integration needed to explore the mains specific integration site of HPV DNA in esophageal cancer and molecular monitoring of the HPV for future prevention researches and also effective therapeutic strategies.

HeLa

10.4236/jct.2019.105029

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TRIM65 promotes vascular smooth muscle cell phenotypic transformation by activating PI3K/Akt/mTOR signaling during atherogenesis

Atherosclerosis (2023)

Zhi‐Xiang Zhou Xiaofeng Ma Wenhao Xiong Zhong Ren Miao Jiang

Calponin

Mural cell

10.1016/j.atherosclerosis.2023.117430

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TRIM65 Promotes Osteogenic Differentiation by Regulating the PI3K/AKT Signaling Pathway

Open Medicine Journal (2024)

Hong-Pu Li Tingting Zeng Zhi‐Xiang Zhou Xiang Xiao An-Yu Liang

Introduction Tripartite motif 65 (TRIM65) is a crucial regulator of cell differentiation, proliferation, migration, invasion, and carcinogenesis. However, its role in osteoporosis (OP) remains unclear. In this study, we evaluated the role of TRIM65 in regulating osteoblast differentiation and calcification. Materials and Methods The role of TRIM65 during the osteogenic differentiation of MC3T3-E1 cells was evaluated. The expression of COL1A1, RUNX2, and OCN was examined using western blot analysis and immunofluorescence staining. The formation of calcium nodules was evaluated using alizarin red staining. Alkaline phosphatase activity was evaluated using ALP staining. Results TRIM65 expression was significantly elevated during the osteogenic differentiation of bone marrow mesenchymal stem and MC3T3-E1 cells. We demonstrated that TRIM65 overexpression enhanced osteogenic differentiation and promoted bone formation in the MC3T3-E1 cells. Conversely, TRIM65 inhibited the osteogenic differentiation and bone formation of the MC3T3-E1 cells. Mechanistically, we found that TRIM65 knockdown in MC3T3-E1 cells up-regulated the phosphorylated protein expression of PI3K and AKT, which was contrary to the results of the TRIM65-overexpression group. Conclusion Our research suggests that TRIM65 is an important osteogenic differentiation and bone formation regulator and offers a therapeutic application for OP.

RUNX2

10.2174/0118742203331864240902064311

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Analysis of the mutations of the APC gene in 79 Chinese patients with colorectal cancer

Int J Genet (2016)

Wentao Ma Xi Chen Tingting Liu Feng Shi Jia‐Jie Hao

Objective To investigate the mutations of adenomatous polyposis coli (APC) gene in Chinese patients with colorectal cancer (CRC). Methods APC gene mutations in the mutation cluster region (MCR) were examined in 79 colorectal tumors by PCR and DNA sequencing. Results Twenty-five (31.6%) somatic mutations were detected in the APC gene as a whole. Among them sixteen (20.3%) were point mutations, which includes, 12 nonsense mutations and 4 missense mutations. The other 9(11%) tumors had frameshift mutations due to a deletion or an insertion. Overall, twenty-one (27%) mutations resulted in the truncation of the APC protein, which accounted for 84% of the total mutations. The mutations in the APC gene were clustered within two small regions of the MCR, that is, codon 1281-1352 and 1411-1465. The frequencies of these two regions were 16.5%(13/79) and 15.2%(12/79), respectively. The mutation rate of codon 1286、1306、1421 and 1450 was relative higher in our cohort. Furthermore, statistical analysis revealed that mutations of the APC gene were not correlated with the age, sex, tumor location, tumor type, histology differentiated degree, depth of invasion, lymph node metastasis, or clinical stage. Conclusion APC gene mutations are frequent in Chinese patients with CRC, and truncating mutation is the predominant type. In addition, there are two small regions with higher mutation rate and four potential mutation hot spots of the APC gene in this cohort. Key words: Colorectal cancer; Adenomatous polyposis coli; Gene mutation

Adenomatous polyposis coli

Nonsense mutation

10.3760/cma.j.issn.1673-4386.2016.03.001

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Suppression of EGFR-STAT3 signaling inhibits tumorigenesis in a lung cancer cell line.

PubMed (2014)

Yongqian Jiang Zhi‐Xiang Zhou JI You-lin

Overactive epidermal growth factor receptor (EGFR) signaling often underlies the rapid expansion of cancerous tissue. EGFR signaling is mediated by transcription factor signal transducer and activator of transcription 3, or STAT3. This study sought to investigate the effects of altered EGFR/STAT3 signal transduction on lung cancer cells in vitro. Lung cancer cells from the cell line A549 were divided into test and control groups. Test group cells were treated with an EGFR monoclonal antibody, Nimotuzumab, while control cells received no treatment. EGFR and STAT3 protein expression, cell apoptosis rate, cell proliferation, cell invasion, and cell division were analyzed and compared. Compared to cells in the control group, lung cancer cells treated with Nimotuzumab showed slowed proliferation rates, accelerated apoptosis, decreased invasion, and arrested cell division (P < 0.05). In conclusion, altered EGFR/STAT3 signaling results in significant changes in the biology of lung cancer cells.

Nimotuzumab

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Multifaceted Nature of HuR in Atherosclerosis Development

Current Medicinal Chemistry (2024)

Yanxia Wang Hongyu Zheng Kun Zhou Hai-Lin Xie Zhong Ren

Abstract: HuR (Human antigen R) is an RNA binding protein (RBP) that specifically binds to certain RNA sequences, influencing post-transcriptional regulation. HuR is primarily involved in tumor regulation, as well as cell growth, proliferation, inflammation, and angiogenesis. HuR is implicated in endothelial activation, smooth muscle proliferation, inflammatory response, macrophage apoptosis, lipid regulation, and autophagy, playing a crucial regulatory role in atherosclerosis. Accumulating evidence suggests that HuR has dual roles in AS. On the one hand, HuR expedites the development of AS by facilitating endothelial activation, smooth muscle proliferation, and inflammation. On the contrary, it exerts beneficial effects by reducing macrophage apoptosis, regulating lipid efflux, and increasing autophagy. In this review, we aim to provide a comprehensive summary of the role of HuR in the development of AS by examining its involvement in cellular mechanisms, inflammation, autophagy, and apoptosis. Additionally, we discuss the mechanisms of drugs that target HuR, with the goal of offering new perspectives for the treatment of AS.

10.2174/0109298673279032231214110313

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