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Monotropein Induced Apoptosis and Suppressed Cell Cycle Progression in colorectal cancer cells

Chinese Journal of Integrative Medicine 2024年第1期30卷 25-33页

作者： GAO Quan LI Lin ZHANG Qi-man SHENG Qin-song ZHANG Ji-liang JIN Li-jun SHANG Rui-yan School of Pharmacy and Department of Medical Oncology the Affiliated Hospital of Hangzhou Normal UniversityHangzhou Normal UniversityHangzhou(311121)China Key Laboratory of Elemene Class Anti-cancer Chinese Medicines Engineering Laboratory of Development and Application of Traditional Chinese MedicinesCollaborative Innovation Center of Traditional Chinese Medicines of Zhejiang ProvinceHangzhou Normal UniversityHangzhou(311121)China Department of colorectal Surgery the First Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhouChina Beijing Tong Ren Tang Chinese Medicine Co. Ltd.Beijing(100000)China Department of Traditional Chinese Medicine Hangzhou Shangcheng District People's HospitalHangzhou(310006)China Department of Gynecology Hangzhou Women's HospitalHangzhou(310008)China

Objective: To determine whether monotropein has an anticancer effect and explore its potential mechanisms against colorectal cancer(CRC) through network pharmacology and molecular docking combined with experimental verification. Methods: Network pharmacology and molecular docking were used to predict potential targets of monotropein against CRC. Cell counting kit assay, plate monoclonal assay and microscopic observation were used to investigate the antiproliferative effects of monotropein on CRC cells HCT116, HT29 and LoVo. Flow cytometry and scratch assay were used to analyze apoptosis and cell cycle, as well as cell migration, respectively in HCT116, HT29, and LoVo cells. Western blotting was used to detect the expression of proteins related to apoptosis, cell cycle, and cell migration, and the expression of proteins key to the Akt pathway. Results: The Gene Ontology and Reactome enrichment analyses indicated that the anticancer potential of monotropein against CRC might be involved in multiple cancer-related signaling pathways. Among these pathways, RAC-beta serine/threonine-protein kinase(Akt1, Akt2), cyclin-dependent kinase 6(CDK6), matrix metalloproteinase-9(MMP9), epidermal growth factor receptor(EGFR), cell division control protein 42 homolog(CDC42) were shown as the potential anticancer targets of monotropein against CRC. Molecular docking suggested that monotropein may interact with the 6 targets(Akt1, Akt2, CDK6, MMP9, EGFR, CDC42). Subsequently, cell activity of HCT116, HT29 and LoVo cell lines were significantly suppressed by monotropein(Pcolorectal cancer by decreasing the expressions of CyclinD1, CDK4 and CDK6, inhibited cell migration by suppressing the expressions of CDC42 and MMP9(Pcancer role through Akt signaling pathway. Conclusions: Monotropein exerts its antitumor

关键词： monotropein Chinese medicine anticancer activity colorectal cancer cells network pharmacology

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Propofol suppressed cell proliferation through inhibition ofSREBP1c-mediated De novo lipogenesis in colorectal cancer cells

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BIOCELL 2024年第12期48卷 1773-1780页

作者： YAJUN CAO SHUANG YIN YIDAN FANG JIEXIAN ZHOU YOUTAN LIU Department of Anesthesiology Shenzhen HospitalSouthern Medical UniversityShenzhen518000China The Third School of Clinical Medicine Southern Medical UniversityGuangzhou510630China Department of Anesthesia Zhuhai Center for Maternal and Child Health CareZhuhai519000China Department of Anesthesia Zhuhai Doumen Maternal and Child Health Care HospitalZhuhai519000China

Background: De novo lipogenesis (DNL) is a critical event for the development of tumors, in the present work,we revealed the role of propofol in colorectal cancer (CRC) cell proliferation. Methods: Western blotting (WB), Real-timePCR, and luciferase combined with chromatin immunoprecipitation (ChIP) were used to identify the mechanismunderlying propofol-modulated cell proliferation in CRC cells. Results: Herein, we showed that propofol suppressedcell proliferation, which was attributed to the inhibition of DNL characterized by reduced fatty acid synthase (FASN),acetyl-coA carboxylase alpha (ACCA), and stearoyl-coA desaturase-1 (SCD1) expression. Mechanically, propofolstimulation decreased sterol regulatory element-binding proteins-1c (SREBP-1c) mature and nuclear translocation,which further decreased SCD1 transactivation confirmed by luciferase and ChIP analysis, while no significantdifference in total SREBP1c was observed. What’s more, supplementation of Monounsaturated fatty acid (MuFA)could reverse the inhibitory effect of propofol on cell proliferation. Conclusion: Taken together, these resultssuggested propofol modulated cell proliferation is dependent on SREBP1c-mediated DNL.

关键词： Propofol SREBP1c De novo lipogenesis Cell proliferation colorectal cancer cells

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Effects of hepatocyte growth factor/scatter factor on the invasion of colorectal cancer cells in vitro

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World Journal of Gastroenterology 2005年第25期11卷 3877-3881页

作者： Hong-WuLi Ji-XianShan DepartmentofOncology FirstAffiliatedHospitalChinaMedicalUniversityShenyang110001LiaoningProvinceChina

AIM: Hepatocyte growth factor (HGF) is a multifunctional growth factor which has pleiotrophic biological effects on epithelial cells, such as proliferation, motogenesis, invas-iveness and morphogenesis. There are few reports about the role of HGF played in the colorectal cancer invasion. In the present study, we tried to investigate the possible mechanism of HGF involved in the invasion of colorectal cancer cells in vitro. METHODS: Matrigel migration assay was used to analyze the migrational ability of Caco-2 and Colo320 in vitro. We detected the mRNA expressive levels of MMP-2, MMP-9 and their natural inhibitors TIMP-1, TIMP-2 in Caco-2 cells by reverse-transcription polymerase chain reaction (PCR) technique. RESULTS: After 48 h incubation, there were notable differences when we compared the migrational numbers of Caco-2 cells in the group of HGF and PD98059 (the inhibitor of p42/p44MAPK) with the control (104.40±4.77 vs 126.80±5.40, t= 7.17, P = 0.002cells to damage the ECM and reach the distant organ and develop metastasis; HGF played the function of promoted-invasion and promoted-metastasis, in which cellular selection was possible.

关键词： HGF colorectal cancer cells Invasion MMPs

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The Inhibitory Effect and Mechanism of Natural Green Tea Extract EGCG in 5-FU-induced Inflammation of colorectal cancer cells

The Inhibitory Effect and Mechanism of Natural Green Tea Ext...

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2021年中国肿瘤标志物学术大会暨第十五届肿瘤标志物青年科学家论坛

作者： Yanhui Li Nanlin Xiang Haiyan Sun Hantao Su Huanliang Liu Xiangling Yang Shenzhen Polytechnic college 中山大学附属第六医院华南理工大学

Background: colorectal cancer(CRC) is the third most common cancer in the world, 5-FU is the most commonly used chemotherapeutic drug for colorectal cancer, simultaneously the side effects of 5-FU,such as inflammation, the extent of the damage could not have been foreseen. we studied the inhibitory effect of epigallocatechin-3-gallate(EGCG) on 5-Fluorouracil(5-FU)-induced inflammation and its underlying mechanism in colorectal cancer(CRC) ***: HCT116 and RKO cells were stimulated with 5-FU and EGCG for 72 h. The changes in cell viability were determined by the CCK-8 assay. It was found that 5-FU indeed significantly attenuated cell viability in a dose-dependent manner in CRC cell lines, while low-dose EGCG had no significant effect on cell viability. CRC cells were cultured with 25μM, 50μM 5-FU and/or 20μM EGCG for 24 *** of inflammatory factors were determined by quantitative Real-Time PCR(qPCR). 5-FU promotes the inflammatory response by inducing a significant increase in the expression of chemokines, such as C-X-C motif chemokine ligand 1 protein(CXCL1) and chemokine(C-C motif)ligand 5(CCL5). Low-dose EGCG significantly reduced 5-FU-induced inflammatory *** blotting was used to determine inflammation-inhibiting effect was mediated by NF-κB and STAT3 signaling pathways. Immunofluorescence also confirmed that in protein ***: Low-dose EGCG can attenuate the 5-FU-induced inflammatory response in CRC cells by inhibiting NF-κB and STAT3 signaling ***: The study indicated that inhibition of NF-κB and STAT3 pathways by low-dose EGCG treatment is essential for inhibition of 5-FU-induced inflammation in human CRC cells.

关键词： Inflammation 5-FU Low-dose EGCG colorectal cancer cells

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Anti-colorectal cancer effects of tripolinolate A from Tripolium vulgare

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Chinese Journal of Natural Medicines 2017年第8期15卷 576-583页

作者： CHEN Lu WANG Wen-Ling SONG Teng-Fei XIE Xin YE Xue-Wei LIANG Ying HUANG Hao-Cai YAN Shi-Lun LIAN Xiao-Yuan ZHANG Zhi-Zhen Ocean College Zhoushan CampusZhejiang UniversityZhoushan 316021China College of Pharmaceutical Sciences Zhejiang UniversityHangzhou 310058China

Tripolinolate A(TLA) is recently identified as a new compound from a halophyte plant Tripolium vulgare and has been shown to have significant in vitro activity against the proliferation of colorectal cancer and glioma cells. This study was designed to further investigate the effects of TLA on the proliferation of human normal cells, and the apoptosis and cell cycle in colorectal cancer cells, and the growth of tumors in the colorectal cancer-bearing animals. The data obtained from this study demonstrated that: 1) TLA had much less cytotoxicity in the human normal cells than the colorectal cancer cells; 2) TLA remarkably induced apoptosis in the human colorectal cancer cells and blocked cell cycle at G2/M phase, and 3) TLA had significant anti-colorectal cancer activity in the tumor-bearing animals.

关键词： Tripolinolate A colorectal cancer cells Apoptosis Cell cycle Anti-colorectal tumor effects

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Elp3 modulates neural crest and colorectal cancer migration requiring functional integrity of HAT and SAM domains

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BIOCELL 2022年第2期46卷 463-470页

作者： XIANGCAI YANG YA XU SHUTING MEI JIEJING LI Department of R&D Biotech&Science Company of UPGuangzhou BranchGuangzhou510000China State Key Laboratory of Genetic Resources and Evolution Kunming Institute of ZoologyChinese Academy of SciencesKunming650223China Laboratory of Developmental Disease and Natural Medicine Medical FacultyKunming University of Science and TechnologyKunming650000China

Cell migration is a finely tuned biological process that often involves epithelial-mesenchymal transition(EMT).EMT is typically characterized by the upregulation of mesenchymal markers such as *** process has been shown to be of critical importance to normal developmental processes,including neural crest migration and ***,similar mechanisms are utilized in disease processes,such as tumor metastasis and ***,EMT and EMT-like processes confer tumor cells with the ability to migrate,invade,and adopt stem cell-like properties that largely account for immunosuppression and tumor ***,identifying sensitive EMT markers may contribute to cancer prognosis and diagnosis in many ***,we showed that Elp3 plays an essential role during neural crest migration by stabilizing *** the current study,we further elucidate the molecular mechanism underlying colorectal cancer *** found that mElp3 exerted an identical function to xElp3 in modulating neural crest migration,and both HAT and SAM domains are imperative during this migratory ***,overexpression of mElp3 in SW480 cells promoted cell migration and invasion,and we further showed that Elp3 stabilized Snail1 requiring integrity of both SAM and HAT *** findings warrant further exploration of the specific target of Elp3 in cancer cells.

关键词： Elp3 Neural crest colorectal cancer cells Migration HAT domain SAM domain

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Approach for mechanism of BH3 domain counterpart BH3I-2' inducing colorectal cancer cell apoptosis

Approach for mechanism of BH3 domain counterpart BH3I-2' ind...

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两岸三地药理学与临床药理学术会议

作者： FENG Wan-yu LIU Yang ZHANG Zhi-cheng (The First Affiliated Hospital, China Medical University, Shenyang 110001, China)

Objective To discuss mechanism of BH3 domain counterpart BH3I-2’inducing colorectal cancer cell *** Detected inhibition ratio and apoptosis of colorectal cancer cells HCT-116,which were treated by BH3I-2’,with microplate reader and flow *** Inhibition ratio of colorectal cancer cells,which were treated by BH3I-2’,could reach about 50%.Ratio of viable apoptotic cell decreased and that of non-viable apoptotic cell increased as time *** BH3I-2’can induce colorectal can- cer cell apoptosis.

关键词： BH3I-2’ apoptosis colorectal cancer cells flow cytometry

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