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miR-30a-5p/PHTF2 axis regulates the tumorigenesis and metastasis of lung adenocarcinoma

BIOCELL 2024年第4期48卷 581-590页

作者： LIJUAN ZHANG QINGYIN MENG LI ZHUANG QUAN GONG XIANDA HUANG XUEQIN LI SHIJUAN LI GUOQIN WANG XICAI WANG Department of Rehabilitation and Palliative Medicine The Third Affiliated Hospital of Kunming Medical UniversityYunnan Cancer HospitalKunmingChina Department of Pathology The Third Affiliated Hospital of Kunming Medical UniversityYunnan Cancer HospitalKunmingChina Emergency Department(Outpatient Chemotherapy Center) The Third Affiliated Hospital of Kunming Medical UniversityYunnan Cancer HospitalKunmingChina Department of Cancer BioTreatment Center The Third Affiliated Hospital of Kunming Medical UniversityYunnan Cancer HospitalKunmingChina Department of Cancer Institute The Third Affiliated Hospital of Kunming Medical UniversityYunnan Cancer HospitalKunmingChina

Background:Lung adenocarcinoma is a very pervasive histological form of lung cancers,and inhibiting metastasis is crucial for effective treatment.In this investigation,we explored the functional interaction of miR-30a-5p and the putative transcription factor 2 of the homeodomain(PHTF2)in dictating the aggressiveness and metastasis of lung adenocarcinoma.Method:We collected clinical samples to evaluate the expression patterns of miR-30a-5p and PHTF2 in lung adenocarcinoma along with normal tissues.Cellular experiments including cell count kit(CCK)-8 growth assay,apoptosis analysis,migration and invasion examinations were performed to assess the aggressiveness of lung adenocarcinoma cells.Furthermore,we examined tumorigenesis and metastasis in a nude mouse model.Results:MiR-30a-5p exhibited downregulation pattern in lung adenocarcinoma samples.Transfection of miR-30a-5p mimic in lung adenocarcinoma cells resulted in the suppression of malignant characteristics.Notably,the administration of miR-30a-5p mimic also curbed tumorigenesis and metastasis of lung adenocarcinoma cells in animal model.Moreover,PHTF2 was found to be a molecular target of miR-30a-5p.Upregulating PHTF2 counteracted the tumor-suppressive effect of the miR-30a-5p mimic.Conclusion:miR-30a-5p functions as a tumor-suppressive molecule while PHTF2 acts as an oncogenic factor in the development and metastasis of lung adenocarcinoma.Therefore,targeting miR-30a-5p and PHTF2 could be developed into a promising therapeutic approach for inhibiting metastasis in lung adenocarcinoma.

关键词： Lung cancer Malignant phenotype Tumor formation Tumor suppressor oncogene

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TM9SF1 promotes bladder cancer cell growth and infiltration

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World Journal of Clinical Oncology 2024年第2期15卷 302-316页

作者： Long Wei Shi-Shuo Wang Zhi-Guang Huang Rong-Quan He Jia-Yuan Luo Bin Li Ji-Wen Cheng Kun-Jun Wu Yu-Hong Zhou Shi Liu Sheng-Hua Li Gang Chen Department of Urology First Affiliated Hospital of Guangxi Medical UniversityNanning 530021Guangxi Zhuang Autonomous RegionChina Department of Pathology First Affiliated Hospital of Guangxi Medical UniversityNanning 530021Guangxi Zhuang Autonomous RegionChina Department of Medical Oncology First Affiliated Hospital of Guangxi Medical UniversityNanning 530021Guangxi Zhuang Autonomous RegionChina

BACKGROUND Bladder cancer(BC)is the most common urological tumor.It has a high recur-rence rate,displays tutor heterogeneity,and resists chemotherapy.Furthermore,the long-term survival rate of BC patients has remained unchanged for decades,which seriously affects the quality of patient survival.To improve the survival rate and prognosis of BC patients,it is necessary to explore the molecular mechanisms of BC development and progression and identify targets for treatment and intervention.Transmembrane 9 superfamily member 1(TM9SF1),also known as MP70 and HMP70,is a member of a family of nine transmembrane superfamily proteins,which was first identified in 1997.TM9SF1 can be expressed in BC,but its biological function and mechanism in BC are not clear.AIM To investigate the biological function and mechanism of TM9SF1 in BC.Overexpression of TM9SF1 increased the in vitro proliferation,migration,and invasion of BC cells by promoting the entry of BC cells into the G2/M phase.Silencing of TM9SF1 inhibited in vitro proliferation,migration,and invasion of BC cells and blocked BC cells in the G1 phase.CONCLUSION TM9SF1 may be an oncogene in BC.

关键词： TM9SF1 Bladder cancer Biological function Cell function assay oncogene

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Understanding the role of transmembrane 9 superfamily member 1 in bladder cancer pathogenesis

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World Journal of Clinical Oncology 2024年第4期15卷 468-471页

作者： Venkata Krishna Vamsi Gade Budhi Singh Yadav Department of Radiotherapy&Oncology Postgraduate Institute of Medical Education and ResearchChandigarh 160012India Department of Radiotherapy&Oncology Regional Cancer CentrePostgraduate Institute of Medical Education and ResearchChandigarh 160012India

In this editorial we comment on the article by Wei et al,published in the recent issue of the World Journal of Clinical Oncology.The authors investigated the role of Transmembrane 9 superfamily member 1(TM9SF1)protein in bladder cancer(BC)carcinogenesis.Lentiviral vectors were used to achieve silencing or overexpression of TM9SF1 gene in three BC cell lines.These cell lines were then subject to cell counting kit 8,wound-healing assay,transwell assay,and flow cytometry.Proliferation,migration,and invasion of BC cells were increased in cell lines subjected to TM9SF1 overexpression.TM9SF1 silencing inhibited proliferation,migration and invasion of BC cells.The authors conclude that TM9SF1 may be an oncogene in bladder cancer pathogenesis.

关键词： Urinary bladder cancer Transmembrane 9 superfamily member 1 gene cell line Lentiviral vectors Wound healing assay oncogene Proliferation Migration

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Dynactin 2 acts as an oncogene in hepatocellular carcinoma through promoting cell cycle progression

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Liver Research 2022年第3期6卷 155-166页

作者： Wenchao Li Jiehuan Chen Zhiyong Xiong Hui Zhou Shaozhuo Huang Jie Ren Bo Liu Taicheng Zhou Kunpeng Hu Department of General Surgery The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdongChina Department of Ultrasound Binhaiwan Central Hospital of DongguanDongguanGuangdongChina Department of Ultrasound The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdongChina Department of Gastroenterological Surgery and Hernia Center The Sixth Affiliated Hospital of Sun Yat-sen UniversityGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor DiseasesGuangzhouGuangdongChina

Background:Dynactin(DCTN)can activate cytoplasmic dynein and drive intracellular organelle transport containing six family members(DCTN1 to DCTN6).The DCTN family has been studied as cancer-related genes or biomarkers in various cancers.Nevertheless,in hepatocellular carcinoma(HCC),the functions and prognostic roles of the DCTN family have been unexplored.Methods:We evaluated the diagnostic and survival effects of DCTN subunits in HCC through bioinformatics analysis and validated the results of bioinformatics by our data to address this problem.Results:The results of bioinformatics analysis found that DCTN2 was a significant prognostic factor in HCC,and high-level DCTN2 can predict poor patient survival in HCC.Cox regression analysis also suggested that DCTN2(hazard ratio=1.748,95%confidence interval 1.190-2.568,P=0.004)is an independent prognostic factor for patient survival.Western blot and quantitative reverse transcriptionpolymerase chain reaction assays confirmed that the protein and mRNA expression levels of DCTN2 were upregulated in HCC cell lines.The proliferation,invasion,and migration were decreased and cell apoptosis was enhanced after DCTN2 was knocked down in Huh7 and Hep3B cells.DCTN2 promoted the cell cycle progression through regulating the expression of cell cycle regulatory proteins cyclindependent kinase 4,Cyclin D1,and p21.Conclusions:We propose that DCTN2 can serve as a prognostic marker for HCC.DCTN2 acts as an oncogene and promotes the cell cycle progression through the G1/S phase-related signaling pathway.

关键词： Dynactin 2(DCTN2) oncogene Hepatocellular carcinoma(HCC) Cell biology Cell cycle

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oncogene addiction and non-oncogene addiction in glioblastoma therapy

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Chinese Medical Journal 2011年第17期124卷 2565-2568页

作者： Kimberly Ng Clark C. Chen Department of Radiation Oncology Dana-Farber Cancer Institute Boston MA USA Division of Neurosurgery Beth Israel Deaconess Medical Center Boston MA USA

INTRODUCTIONGlioblastoma is the most common form of primary brain tumor. The incidence of this tumor is fairly low, with 2-3 cases per 100 000 people in Europe and North America.

关键词： oncogene addiction glioblastoma

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Molecular Cloning of a Novel Mouse Testis-specific Spermatogenic Cell Apoptosis Inhibitor Gene mTSARG7 as a Candidate oncogene

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Acta Biochimica et Biophysica Sinica 2005年第6期37卷 396-405页

作者： Xiao-Jun TAN Xiao-Wei XING Lu-Yun LI Zhao-Di WU Chang-Gao ZHONG Dong-Song NIE Jun-Jiang FU Yang XIANG Yun DENG Guang-Xiu LU Institute of Human Reproductive and Stem cell Engineering, Central South University, Changsha 410078,China Institute of Human Reproductive and Stem cell Engineering Central South University Changsha 410078 China

A novel mouse gene,mTSARG7(GenBank accession No.AY489184),with a full cDNA lengthof 2279 bp and containing 12 exons and 11 introns,was cloned from a mouse expressed sequence tag(GenBank accession No.BE644543)that was significantly up-regulated in cryptorchidism.The gene waslocated in mouse chromosome 8A1.3 and encoded a protein containing 403 amino acid residues that was anew member of the acyltransferase family because the sequence contained the highly conserved phosphateacyltransferase(PlsC)domain existing in all acyltransferase-like proteins.The mTSARG7 protein and AU041707protein shared 83.9% identity in 402 amino acid residues.Expression of the mTSARG7 gene was restrictedto the mouse testis.The results of the in situ hybridization analysis revealed that the mTSARG7 mRNA wasexpressed in mouse spermatogonia and spermatocytes.Subcellular localization studies showed that the EGFP-tagged mTSARG7 protein was localized in the cytoplasm of GC-1 spg cells.The mTSARG7 mRNA expres-sion was initiated in the mouse testis in the second week after birth,and the expression level increasedsteadily with spermatogenesis and sexual maturation of the mouse.The results of the heat stress experimentshowed that the mTSARG7 mRNA expression gradually decreased as the heating duration increased.ThepcDNA3.1 Hygro(-)/mTSARG7 plasmid was constructed and introduced into GC-1 spg cells by liposometransfection.The mTSARG7 can accelerate GC-1 spg cells,causing them to traverse the S-phase and enterthe G2-phase,compared with the control group where this did not occur as there was no transfection ofmTSARG7.In conclusion,our results suggest that this gene may play an important role in spermatogenesisand the development of cryptorchid testes,and is a testis-specific apoptosis candidate oncogene.

关键词： mTSARG7 testis spermatogenesis oncogene

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SHANK2 is a frequently amplified oncogene with evolutionarily conserved roles in regulating Hippo signaling

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Protein & Cell 2021年第3期12卷 174-193页

作者： Liang Xu Peixue Li Xue Hao Yi Lu Mingxian Liu Wenqian Song Lin Shan Jiao Yu Hongyu Ding Shishuang Chen Ailing Yang Yi Arial Zeng Lei Zhang Hai Jiang State Key Laboratory of Cell Biology CAS Center for Excellence in Molecular Cell ScienceShanghai Institute of Biochemistry and Cell BiologyChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghai 200031China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China Bio-Research Innovation Center Shanghai Institute of Biochemistry and Cell BiologyChinese Academy of SciencesSuzhou 215121China

Dysfunction of the Hippo pathway enables cells to evade contact inhibition and provides advantages for cancerous overgrowth.However,for a significant portion of human cancer,how Hippo signaling is perturbed remains unknown.To answer this question,we performed a genome-wide screening for genes that affect the Hippo pathway in Drosophila and cross-referenced the hit genes with human cancer genome.In our screen,Prosap was identified as a novel regulator of the Hippo pathway that potently affects tissue growth.Interestingly,a mammalian homolog of Prosap,SHANK2,is the most frequently amplified gene on 11 q13,a major tumor amplicon in human cancer.Gene amplification profile in this 11q13 amplicon clearly indicates selective pressure for SHANK2 amplification.More importantly,across the human cancer genome,SHANK2 is the most frequently amplified gene that is not located within the Myc amplicon.Further studies in multiple human cell lines confirmed that SHANK2 overexpression causes deregulation of Hippo signaling through competitive binding for a LATS1 activator,and as a potential oncogene,SHANK2 promotes cellular transformation and tumor formation in vivo.In cancer cell lines with deregulated Hippo pathway,depletion of SHANK2 restores Hippo signaling and ceases cellular proliferation.Taken together,these results suggest that SHANK2 is an evolutionarily conserved Hippo pathway regulator,commonly amplified in human cancer and potently promotes cancer.Our study for the first time illustrated oncogenic function of SHANK2,one of the most frequently amplified gene in human cancer.Furthermore,given that in normal adult tissues,SHANK2 s expression is largely restricted to the nervous system,SHANK2 may represent an interesting target for anticancer therapy.

关键词： SHANK2 oncogene Hippo signaling cancer

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Identification of APEX2 as an oncogene in liver cancer

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World Journal of Clinical Cases 2020年第14期8卷 2917-2929页

作者： Ru Zheng Heng-Liang Zhu Bing-Ren Hu Xiao-Jiao Ruan Hua-Jie Cai Department of General Surgery The First Affiliated Hospital of Wenzhou Medical UniversityWenzhou 325000Zhejiang ProvinceChina Department of General Surgery Shenzhen University General HospitalShenzhen 518107Guangdong ProvinceChina

BACKGROUND DNA damage is one of the critical contributors to the occurrence and development of some cancers.APEX1 and APEX2 are the most important molecules in the DNA damage,and APEX1 has been identified as a diagnostic and prognostic biomarker in liver hepatocellular carcinoma(LIHC).However,the expression of APEX2 and its functional mechanisms in LIHC are still unclear.AIM To examine the expression of APEX2 and the potential mechanism network in LIHC.METHODS We conducted a pan-cancer analysis of the expression of APEX1 and APEX2 using the interactive TIMER tool.GEO datasets,including GSE14520,GSE22058,and GSE64041,were used to compare the APEX2 expression level in tumor tissues and adjacent non-tumor tissues.Then,we calculated the 5-year survival rate according to the web-based Kaplan-Meier analysis.We included the TCGA liver cancer database in GSEA analysis based on the high and low APEX2 expression,showing the potential mechanisms of APEX2 in LIHC.After that,we conducted Pearson correlation analysis using GEPIA2.Next,we performed quantitative polymerase chain reaction(qPCR)assay to examine the APEX2 levels in normal liver cell line LO2 and several liver cancer cell lines,including HepG2,Huh7,SMMC7721,and HCCLM3.APEX2 in HCCLM3 cells was knocked down using small interfering RNA.The role of APEX2 in cell viability was confirmed using CCK-8.Dualluciferase reporter assay was performed to examine the promoter activity of CCNB1 and MYC.RESULTS APEX1 and APEX2 are both highly expressed in the tumor tissues of BLCA,BRCA,CHOL,COAD,ESCA,HNSC,LIHC,LUAD,LUSC,READ,and STAD.APEX2 overexpression in LIHC was validated using GSE14520,GSE22058,and GSE64041 datasets.The survival analysis showed that LIHC patients with high expression of APEX2 had a lower overall survival rate,even in the AJCC T1 patients.High level of APEX2 could indicate a lower overall survival rate in patients with or without viral hepatitis.The GSEA analysis identified that kinetochore and spindle microtubules are the two main cellular components of APEX2 i

关键词： APEX2 High expression Worse prognosis Pro-oncogenic pathway oncogene Liver cancer

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Analysis of cyclin E co-expression genes reveals nuclear transcription factor Y subunit alpha is an oncogene in gastric cancer

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Chronic Diseases and Translational Medicine 2019年第1期5卷 44-52页

作者： Liang-Yu Bie Dan Li Yu Mu Sheng Wang Bei-Bei Chen Hui-Fang Lyu Li-Li Han Cai-Yun Nie Chang-Cheng Yang Lin Wang Chuan-Chuan Ren Wei-Jie Zhang Ping Guo Feng Shi Qing-Xia Fan Liu-Xing Wang Xiao-Bing Chen Su-Xia Luo Department of Oncology Affiliated Cancer Hospital of Zhengzhou University/Henan Cancer Hospital Zhengzhou Henan 450008 China Department of General Surgery Affiliated Cancer Hospital of Zhengzhou University/Henan Cancer Hospital Zhengzhou Henan 450008 China Department of Combined Traditional Chinese and Western Medicine Oncology Affiliated Cancer Hospital of Zhengzhou University/Henan Cancer Hospital Zhengzhou Henan 450008 China Department of Radiation Oncology Zhengzhou People's Hospital Zhengzhou Henan 450008 China Department of Urology First Affiliated Hospital of Zhengzhou University Zhengzhou Henan 450052 China Department of Medical Oncology First Affiliated Hospital of Zhengzhou University Zhengzhou Henan 450052 China Department of Oncology The First Affiliated Hospital of Nanyang Medical College Nanyang Henan 473000 China Department of Thoracic Surgery The First Affiliated Hospital of Nanyang Medical College Nanyang Henan 473000 China

Objective: To explore genes potentially co-expressed with cyclin E in gastric cancer and discover possible targets for gastric cancer treatment. Methods: The Cancer Genome Atlas (TCGA) stomach adenocarcinoma sequencing data were used to predict genes co-expressed with cyclin E. Co-expression genes predicted by cBioPortal online analysis with Pearson correlation coefficient ≥0.4 were analyzed by gene ontology (GO) enrichment annotation using the PANTHER online platform (Ver. 7). Interactions between proteins encoded by these genes were analyzed using the STRING online platform (Ver. 10.5) and Cytoscape software (Ver. 3.5.1). Genes displaying a high degree of connection were analyzed by transcription factor enrichment prediction using FunRich software (Ver. 3). The significant transcription factor and cyclin E expression levels and their impact on gastric cancer progression were analyzed by Western blotting and Kaplan-Meier survival curve analysis. Results: After filtering the co-expression gene prediction results, 78 predicted genes that included 73 protein coding genes and 5 non-coding genes with Pearson correlation coefficient ≥0.4 were selected. The expressions of the genes were considered to be correlated with cyclin E expression. Among the 78 genes co-expressed with cyclin E, 19 genes at the central of the regulatory network associated with cyclin E were discovered. Nuclear transcription factor Y subunit alpha (NF-YA) was identified as a significant transcription factor associated with cyclin E co-expressing genes. Analysis of specimen donors’ clinical records revealed that high expression of NF-YA tended to be associated with increased cyclin E expression. The expression of both was associated with progression of gastric cancer. Western blotting results showed that compared with normal tissues, NF-YA and cyclin E were highly expressed in tumor tissues (P < 0.001). Survival curve analysis clearly demonstrated relatively poor overall survival of gastric cancer patients with high cyclin E or high NF-YA expressi

关键词： Cyclin E Nuclear transcription factor Y subunit alpha oncogene Gastric cancer

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DEAD-box RNA helicases with special reference to p68:Unwinding their biology,versatility,and therapeutic opportunity in cancer

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Genes & Diseases 2023年第4期10卷 1220-1241页

作者： Shaheda Tabassum Mrinal K.Ghosh Cancer Biology and Inflammatory Disorder Division Council of Scientific and Industrial Research-Indian Institute of Chemical Biology(CSIR-IICB)TRUE CampusSalt LakeKolkata 700091India

In the era of advancement,the entire world continues to remain baffled by the increased rate of progression of cancer.There has been an unending search for novel thera-peutic targets and prognostic markers to curb the oncogenic scenario.The DEAD-box RNA he-licases are a large family of proteins characterized by their evolutionary conserved D-E-A-D(Asp-Glu-Ala-Asp)domain and merit consideration in the oncogenic platform.They perform multidimensional functions in RNA metabolism and also in the pathology of cancers.Their bio-logical role ranges from ribosome biogenesis,RNA unwinding,splicing,modification of second-ary and tertiary RNA structures to acting as transcriptional coactivators/repressors of various important oncogenic genes.They also play a crucial role in accelerating oncogenesis by pro-moting cell proliferation and metastasis.DDX5(p68)is one of the archetypal members of this family of proteins and has gained a lot of attention due to its oncogenic attribute.It is found to be overexpressed in major cancer types such as colon,brain,breast,and prostate cancer.It exhibits its multifaceted nature by not only coactivating genes implicated in cancers but also mediating crosstalk across major signaling pathways in cancer.Therefore,in this review,we aim to illustrate a comprehensive overview of DEAD-box RNA helicases especially p68 by focusing on their multifaceted roles in different cancers and the various signaling pathways affected by them.Further,we have also briefly discoursed the therapeutic interventional approaches with the DEAD-box RNA helicases as the pharmacological targets for designing in-hibitors to pave way for cancer therapy.

关键词： Cancer DDX5 DEAD-box RNA helicases Gene expression oncogene Signaling Therapy Transcription factor

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