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| 1 | Bevacizumab biosimilar LY01008 compared with bevacizumab(Avastin)as first-line treatment for Chinese patients with unresectable,metastatic,or recurrent non-squamous non-small-cell lung cancer:A multicenter,randomized,double-blinded,phase Ⅲ trial显示文摘Background:Previous studies have demonstrated the preclinical pharmacological and toxicological consistency,and clinical pharmacokinetic equivalence of bevacizumab biosimilar LY01008 with reference bevacizumab(Avastin).This randomized controlled trial aimed to compare the efficacy and safety of LY01008 with Avastin in first-line treatment of Chinese patients with advanced or recurrent non-squamous non-small cell lung cancer(NSCLC).Methods:StageⅢB-ⅣNSCLC patients with evaluable lesions,good physical status,and adequate organ functions from 67 centers across China were randomized in a ratio of 1:1 to receive LY01008 or Avastin 15 mg/kg intravenously in combination with paclitaxel/carboplatin(combined treatment)for 4-6 cycles,followed by maintenance monotherapy with LY01008 until disease progression,intolerable toxicity,or death.The primary endpoint was objective response rate(ORR)in accordance with Response Evaluation Criteria in Solid Tumors(RECIST)version 1.1 confirmed by independent radiological review committees(IRRC).Secondary endpoints included disease control rate(DCR),duration of response(DoR),progression-free survival(PFS),overall survival(OS),and safety.This study was registered in Clinical Trials.gov(NCT03533127).Results:Between December 15^(th),2017,and May 15^(th),2019,a total of 649 patients were randomized to the LY01008(n=324)or Avastin(n=325)group.As of September 25th,2019 for primary endpoint analysis,589 patients received ORR evaluation,with a median number of combined treatment cycles of 5(range 1-6)andmedian duration of treatment of 3.0(range 0.0-5.1)months.ORRof responseevaluable patients in the LY01008 and Avastin groups were 48.5% and 53.0%,respectively.The stratified ORR ratio was 0.91(90%CI 0.80-1.04,within the prespecified equivalence margin of 0.75-1.33).Up to May 15^(th),2020,with a median follow-up of 13.6(range 0.8-28.4)months,no notable differences in DCR,median DoR,median PFS,median OS,and 1-year OS rate were observed between the LY01008 and Avastin groups.There were no clinically meaningful differences in safety and immunogenicity across treatment groups.Conclusions:LY01008 demonstrated similarity to Avastin in terms of efficacy and safety in Chinese patients with advanced or recurrent non-squamous NSCLC.LY01008 combined with paclitaxel/carboplatin is expected to become a new treatment option for unresectable,metastatic,LY01008 and Avastin groups.There were no clinically meaningful differences in safety and immunogenicity across treatment groups.Conclusions:LY01008 demonstrated similarity to Avastin in terms of efficacy and safety in Chinese patients with advanced or recurrent non-squamous NSCLC.LY01008 combined with paclitaxel/carboplatin is expected to become a new treatment option for unresectable,metastatic,or recurrent non-squamous NSCLC patients in the first-line setting. | Yuankai Shi Kaijian Lei Yuming Jia Bingqiang Ni Zhiyong He Minghong Bi Xicheng Wang Jianhua Shi Ming Zhou Qian Sun Guolei Wang Dongji Chen Yongqian Shu Lianke Liu Zhongliang Guo Yong Liu Junquan Yang Ke Wang Ke Xiao LinWu Tienan Yi Debin Sun Mafei Kang Tianjiang Ma Yimin Mao Jinsheng Shi Tiegang Tang Yan Wang Puyuan Xing Dongqing Lv Wangjun Liao Zhiguo Luo Bin Wang Xiaohong Wu Xiaoli Zhu Shuhua Han Qisen Guo Rongyu Liu Zhiwei Lu Jianyong Zhang Jian Fang Changlu Hu Yinghua Ji Guolong Liu Hong Lu Dedong Wu Junhong Zhang Shuyang Zhu Zheng Liu Wensheng Qiu Feng Ye Yan Yu Yanqiu Zhao Qinhong Zheng Jun Chen Zhanyu Pan Yiping Zhang Wenjuan Lian Bo Jiang Bo Qiu Guojun Zhang Hua Zhang Yanju Chen Yuan Chen Hongbing Duan Manxiang Li Shengming Liu Lijun Ma Hongming Pan Xia Yuan Xueli Yuan Yulong Zheng Emei Gao Li Zhao Shumin Wang Can Wu | 2021 | Cancer Communications2021，41，9： | 5 |
| 2 | Depression accelerates gastric cancer invasion and metastasis by inducing a neuroendocrine phenotype via the catecholamine/β_(2)-AR/MACC1 axis显示文摘Background:Depression is a common,easily ignored,accompanied disease of gastric cancer(GC)patients and is often observed with elevated plasma catecholamine levels.Depression frequently promotes GC progression and leads to poor clinical outcomes;however,the molecular mechanisms underlying depression-induced GC progression remain poorly understood.We aimed to study the effects of depression on GC progression and explore possible mechanisms mediating the action of depression-associated catecholamines on GC.Methods:Depression states of GC patients were graded using the Patient Health Questionnaire-9,and plasma catecholamine levels were examined by high performance liquid chromatography coupled with tandem mass spectrometry.Migrative and invasive GC cells were examined using transwell assays,and metastatic GC niches were imaged using bioluminescence technology in a depression mouse model established with chronic unpredictable mild stress.Mouse depression-like behaviors were assessed through sucrose preference,forced swimming,and tail suspension tests.Characteristics of the neuroendocrine phenotype were observed via RT-PCR,Western blotting,flow cytometry,and transmission electron microscopy.Results:Fifty-one GC patients(age:53.61±1.79 years;cancer duration:3.71±0.33 months;depression duration:2.37±0.38 months;male-to-female ratio:1.55:1)were enrolled in the study.Depression grade was significantly higher in GC patients showing higher plasma levels of catecholamines(epinephrine:P=0.018;noradrenaline:P=0.009),higher oncogene metastasis-associated in colon cancer-1(MACC1)level(P=0.018),and metastasis(P<0.001).Further,depression-associated catecholamine specifically bound to the beta-2 adrenergic receptor(β_(2)-AR)and upregulated MACC1 expression,and thus promoting neuroendocrine phenotypic transformation through direct binding betweenMACC1 and synaptophysin.Eventually,the neuroendocrine phenotypic transformation accelerated GC invasion in vitro and metastasis in vivo.However,β_(2)-AR antagonist ICI-118,551 or MACC1 silencing effectively blocked the catecholamineinduced neuroendocrine phenotypic transformation and eliminated depressionenhanced GC migration and invasion.Moreover,β_(2)-AR blocking or MACC1 silencing prevented GC metastasis attributed to a neuroendocrine phenotype in a depression mouse model.Conclusions:Catecholamine-induced neuroendocrine phenotypes of GC cells led to depression-accelerated GC invasion and metastasis via the β_(2)-AR/MACC1 axis,while β_(2)-AR antagonist or MACC1 silencing could reverse it,showing promising potential therapeutic strategies for improving the outcome of GC patients with comorbid depression. | Changqie Pan Jianhua Wu Siting Zheng Huiying Sun Yisheng Fang Zhenhua Huang Min Shi Li Liang Jianping Bin Yulin Liao Jinzhang Chen Wangjun Liao | 2021 | Cancer Communications2021，41，10： | 4 |
| 3 | The prognostic significance of non-sentinel lymph node metastasis in cutaneous and acral melanoma patients—A multicenter retrospective study显示文摘Background:Whether non-sentinel lymph node(SLN)-positive melanoma patients can benefit from completion lymph node dissection(CLND)is still unclear.The current study was performed to identify the prognostic role of nonSLN status in SLN-positive melanoma and to investigate the predictive factors of non-SLN metastasis in acral and cutaneous melanoma patients.Methods:The records of 328 SLN-positive melanoma patients who underwent radical surgery at four cancer centers from September 2009 to August 2017 were reviewed.Clinicopathological data including age,gender,Clark level,Breslow index,ulceration,the number of positive SLNs,non-SLN status,and adjuvant therapy were included for survival analyses.Patients were followed up until death or June 30,2019.Multivariable logistic regression modeling was performed to identify factors associated with non-SLN positivity.Log-rank analysis and Cox regression analysis were used to identify the prognostic factors for disease-free survival(DFS)and overall survival(OS).Results:Among all enrolled patients,220(67.1%)had acral melanoma and 108(32.9%)had cutaneous melanoma.The 5-year DFS and OS rate of the entire cohort was 31.5%and 54.1%,respectively.More than 1 positive SLNs were found in 123(37.5%)patients.Positive non-SLNs were found in 99(30.2%)patients.Patients with positive non-SLNs had significantly worse DFS and OS(log-rank P<0.001).Non-SLN status(P=0.003),number of positive SLNs(P=0.016),and adjuvant therapy(P=0.025)were independent prognostic factors for DFS,while non-SLN status(P=0.002),the Breslow index(P=0.027),Clark level(P=0.006),ulceration(P=0.004),number of positive SLNs(P=0.001),and adjuvant therapy(P=0.007)were independent prognostic factors for OS.The Breslow index(P=0.020),Clark level(P=0.012),and number of positive SLNs(P=0.031)were independently related to positive non-SLNs and could be used to develop more personalized surgical strategy.Conclusions:Non-SLN-positive melanoma patients had worse DFS and OS even after immediate CLND than those with non-SLN-negative melanoma.The Breslow index,Clark level,and number of positive SLNs were independent predictive factors for non-SLN status. | Wei Sun Yu Xu JiLong Yang ZhiChao Liao Tao Li Kai Huang Poulam Patel WangJun Yan Yong Chen | 2020 | Cancer Communications2020，40，11： | 2 |
| 4 | Current management of chemotherapy-induced neutropenia in adults:key points and new challenges显示文摘Chemotherapy-induced neutropenia(CIN)is a potentially fatal and common complication in myelosuppressive chemotherapy.The timing and grade of CIN may play prognostic and predictive roles in cancer therapy.CIN is associated with older age,poor functional and nutritional status,the presence of significant comorbidities,the type of cancer,previous chemotherapy cycles,the stage of the disease,specific chemotherapy regimens,and combined therapies.There are many key points and new challenges in the management of CIN in adults including:(1)Genetic risk factors to evaluate the patient’s risk for CIN remain unclear.However,these risk factors urgently need to be identified.(2)Febrile neutropenia(FN)remains one of the most common reasons for oncological emergency.No consensus nomogram for FN risk assessment has been established.(3)Different assessment tools[e.g.,Multinational Association for Supportive Care in Cancer(MASCC),the Clinical Index of Stable Febrile Neutropenia(CISNE)score model,and other tools]have been suggested to help stratify the risk of complications in patients with FN.However,current tools have limitations.The CISNE score model is useful to support decision-making,especially for patients with stable FN.(4)There are still some challenges,including the benefits of granulocyte colony stimulating factor treatment and the optimal antibiotic regimen in emergency management of FN.In view of the current reports,our group discusses the key points,new challenges,and management of CIN. | Committee of Neoplastic Supportive-Care(CONS),China Anti-Cancer Association Committee of Clinical Chemotherapy,China Anti-Cancer Association Yi Ba Yuankai Shi Wenqi Jiang Jifeng Feng Ying Cheng Li Xiao Qingyuan Zhang Wensheng Qiu Binghe Xu Ruihua Xu Bo Shen Zhiguo Luo Xiaodong Xie Jianhua Chang Mengzhao Wang Yufu Li Yuerong Shuang Zuoxing Niu Bo Liu Jun Zhang Li Zhang Herui Yao Conghua Xie Huiqiang Huang Wangjun Liao Gongyan Chen Xiaotian Zhang Hanxiang An Yanhong Deng Ping Gong Jianping Xiong Qinghua Yao Xin An Cheng Chen Yanxia Shi Jialei Wang Xiaohua Wang Zhiqiang Wang Puyuan Xing Sheng Yang Chenfei Zhou | 2020 | Cancer Biology & Medicine2020，17，4： | 2 |
| 5 | Metastasis‐associated in colon cancer‐1 upregulation predicts a poor prognosis of gastric cancer, and promotes tumor cell proliferation and invasion显示文摘 | Lin Wang Yajun Wu Li Lin Pengmin Liu Hui Huang Wenjun Liao Dayong Zheng Qiang Zuo Li Sun Na Huang Min Shi Yulin Liao Wangjun Liao | 2013 | Cancer2013，，6： | 1 |
| 6 | A knockdown of Maml1 that results in melanoma cell senescence promotes an innate and adaptive immune response显示文摘 | Shijun Kang Jianmin Xie Jingxia Miao Rong Li Wangjun Liao Rongcheng Luo | 2013 | Cancer Immunology, Immunotherapy2013，，： | 1 |
| 7 | Metastasis-associated in colon cancer-1 upregulates vascular endothelial growth factor-C/D to promote lymphangiogenesis in human gastric cancer显示文摘 | Li Sun Jiangman Duan Yaqi Jiang Lin Wang Na Huang Li Lin Yulin Liao Wangjun Liao | 2014 | Cancer Letters2014，，： | 1 |
| 8 | Evolution of tumor microenvironment in colorectal liver metastases under treatment stress显示文摘Dear editor,The tumor microenvironment(TME)heavily impacts disease biology and may influence responses to systemic treatments,and thereby,affects patients’prognosis.In our previous study,we found that immune features could predict prognosis and guide the therapy choices for stage I-III colon cancer[1,2].Increasing evidence shows that therapyinduced TME changes can promote tumor progression,metastasis,and the development of resistance[3,4].However,the TME dynamics in colorectal liver metastases(CRLM)under treatment are still incompletely clear. | Na Huang Dongqiang Zeng Xiaoxiang Rong Chunlin Wang Zhenzhen Wu Jian Guo Yuqi Wang Jin Li Jing Li Jiao Wang Siting Zheng Genjie Huang Jianping Bin Yulin Liao Qian Li Xin Yi Wangjun Liao Min Shi | 2022 | Cancer Communications2022，42，5： | 1 |
| 9 | Metastasis‐associated in colon cancer‐1 upregulation predicts a poor prognosis of gastric cancer, and promotes tumor cell proliferation and invasion显示文摘 | Lin Wang Yajun Wu Li Lin Pengmin Liu Hui Huang Wenjun Liao Dayong Zheng Qiang Zuo Li Sun Na Huang Min Shi Yulin Liao Wangjun Liao | 2013 | Int J Cancer2013，，6： | 1 |
| 10 | Cebpa is essential for the embryonic myeloid progenitor and neutrophil maintenance in zebrafish显示文摘In vertebrates, myeloid cells arise from multiple waves of development: the first or embryonic wave of myelopoiesis initiates early from non-hematopoietic stem cell(HSC) precursors and gives rise to myeloid cells transiently during early development; whereas the second or adult wave of myelopoiesis emerges later from HSCs and produces myeloid cells continually during fetal and adult life. In the past decades, a great deal has been learnt about the development of myeloid cells from adult myelopoiesis, yet the genetic network governing embryonic myelopoiesis remains poorly defined. In this report, we present an in vivo study to delineate the role of Cebpa during zebrafish embryonic myelopoiesis. We show that embryonic myelopoiesis in cebpa-deficient zebrafish mutants initiates properly but fails to produce macrophages and neutrophils. The lack of macrophages and neutrophils in the mutants is largely attributed to the cell cycle arrest of embryonic myeloid progenitors, resulting in the impairment of their maintenance and subsequent differentiation. We further show that Cebpa, perhaps acting cooperatively with Runx1, plays a critical role in embryonic neutrophil maintenance. Our findings reveal a new role of Cebpa in embryonic myelopoiesis. | Yimei Dai Lu Zhu Zhibin Huang Minyu Zhou Wan Jin Wei Liu Mengchang Xu Tao Yu Yiyue Zhang Zilong Wen Wangjun Liao Wenqing Zhang | 2016 | Journal of Genetics and Genomics2016，43，10： | 0 |
| 11 | High baseline tumor burden-associated macrophages promote an immunosuppressive microenvironment and reduce the efficacy of immune checkpoint inhibitors through the IGFBP2-STAT3-PD-L1 pathway显示文摘Background:Several clinical studies have uncovered a negative correlation between baseline tumor burden and the efficacy of immune checkpoint inhibitor(ICI)treatment.This study aimed to uncover the specific mechanisms underlying the difference in sensitivity to ICI treatment between tumors with high(HTB)and low(LTB)tumor burden.Methods:For in vivo studies,several mouse models of subcutaneous tumors were established,and transcriptome sequencing,immunohistochemistry,and flow cytometry assays were used to detect the immune status in these subcutaneous tumors.For in vitro experiments,co-culture models,cytokine antibody arrays,western blotting,flow cytometry,and enzyme-linked immunosorbent assays were used to explore the underlying molecular mechanisms Results:We found that MC38 or B16 subcutaneous tumors from the HTB group did not show any response to anti-programmed cell death protein-1(PD-1)therapy.Through flow cytometry assays,we found that the infiltration with CD8^(+)T cellswas significantly decreasedwhereasM2-like macrophageswere enriched in subcutaneous tumors of HTB groups compared with those of LTB group.These changes were not affected by the initial number of injected tumor cells or tumor age,nor could they be reversed by surgical tumor reduction.Intraperitoneal colony-stimulating factor 1 receptor(CSF-1R)inhibitor PLX3397 injection at different time points of tumor growth only had an effect when administered in the early tumor stage to maintain the“heat”of the tumor microenvironment during the process of tumor growth,thereby achieving a response to ICI treatment when the tumor grew to a large size.Mechanistically,we found that insulin-like growth factor binding protein 2(IGFBP2)expression levelswere significantly elevated in HTB tumor tissues.IGFBP2 promoted the programmed death-ligand 1(PD-L1)expression in M2-like macrophages by activating signal transducer and activator of transcription 3(STAT3),and PD-L1^(+)M2-likemacrophages exerted an immunosuppressive effect by inhibiting the proliferation and activation of CD8^(+)T cells in a PD-L1-dependent fashion.Conclusions:This study suggested that the low efficacy of ICI treatment in HTB tumors is mainly attributed to the intratumoral accumulation of PD-L1^(+)M2-like macrophages via the IGFBP2-STAT3-PD-L1 signaling pathway and their substantial inhibitory effects on T cell proliferation and activation. | Zhaowei Wen Huiying Sun Zhihua Zhang Yannan Zheng Siting Zheng Jianping Bin Yulin Liao Min Shi Rui Zhou Wangjun Liao | 2023 | Cancer Communications2023，43，5： | 0 |
| 12 | VEGFR2 inhibition hampers breast cancer cell proliferation via enhanced mitochondrial biogenesis显示文摘Objective:Vascular endothelial growth factor(VEGF),apart from its predominant roles in angiogenesis,can enhance cancer cell proliferation,but its mechanisms remain elusive.The purpose of the present study was therefore to identify how VEGF regulates cancer cell proliferation.Methods:VEGF effects on cancer cell proliferation were investigated with the VEGF receptor 2 inhibitor,Ki8751,and the breast cancer cell lines,MCF-7 and MDA-MB-231,using flow cytometry,mass spectrometry,immunoblotting,and confocal microscopy.Data were analyzed using one-way analysis of variance followed by Tukey’s multiple comparison test.Results:VEGF blockade by Ki8751 significantly reduced cancer cell proliferation,and enhanced breast cancer cell apoptosis.Mass spectrometric analyses revealed that Ki8751 treatment significantly upregulated the expression of mitochondrial proteins,suggesting the involvement of mitochondrial biogenesis.Confocal microscopy and flow cytometric analyses showed that Ki8751 treatment robustly increased the mitochondrial masses of both cancer cells,induced endomitosis,and arrested cancer cells in the high aneuploid phase.VEGFR2 knockdown by sh RNAs showed similar effects to those of Ki8751,confirming the specificity of Ki8751 treatment.Enhanced mitochondrial biogenesis increased mitochondrial oxidative phosphorylation and stimulated reactive oxygen species(ROS)production,which induced cancer cell apoptosis.Furthermore,Ki8751 treatment downregulated the phosphorylation of Akt and PGC1α,and translocated PGC1αinto the nucleus.The PGC1αalterations increased mitochondrial transcription factor A(TFAM)expression and subsequently increased mitochondrial biogenesis.Conclusions:VEGF enhances cancer cell proliferation by decreasing Akt-PGC1α-TFAM signaling-mediated mitochondrial biogenesis,ROS production,and cell apoptosis.These findings suggested the anticancer potential of Ki8751 via increased mitochondrial biogenesis and ROS production. | Hao Ni Min Guo Xuepei Zhang Lei Jiang Shuai Tan Juan Yuan Huanhuan L Cui Yanan Min Junhao Zhang Susanne Schlisio Chunhong Ma Wangjun Liao Monica Nister Chunlin Chen Shuijie Li Nailin Li | 2021 | Cancer Biology & Medicine2021，18，1： | 0 |
| 13 | Glutamine metabolic microenvironment drives M2 macrophage polarization tomediate trastuzumab resistance in HER2-positive gastric cancer显示文摘Background:Trastuzumab is a first-line targeted therapy for human epidermal growth factor receptor-2(HER2)-positive gastric cancer.However,the inevitable occurrence of acquired trastuzumab resistance limits the drug benefit,and there is currently no effective reversal measure.Existing researches on the mechanism of trastuzumab resistance mainly focused on tumor cells themselves,while the understanding of the mechanisms of environment-mediated drug resistance is relatively lacking.This study aimed to further explore the mechanisms of trastuzumab resistance to identify strategies to promote survival in these patients.Methods:Trastuzumab-sensitive and trastuzumab-resistant HER2-positive tumor tissues and cells were collected for transcriptome sequencing.Bioinformatics were used to analyze cell subtypes,metabolic pathways,and molecular signaling pathways.Changes in microenvironmental indicators(such as macrophage,angiogenesis,and metabolism)were verified by immunofluorescence(IF)and immunohistochemical(IHC)analyses.Finally,a multi-scale agent-based model(ABM)was constructed.The effects of combination treatment were further validated in nude mice to verify these effects predicted by the ABM.Results:Based on transcriptome sequencing,molecular biology,and in vivo experiments,we found that the level of glutamine metabolism in trastuzumabresistant HER2-positive cells was increased,and glutaminase 1(GLS1)was significantly overexpressed.Meanwhile,tumor-derived GLS1 microvesicles drove M2macrophage polarization.Furthermore,angiogenesis promoted trastuzumab resistance.IHC showed high glutamine metabolism,M2 macrophage polarization,and angiogenesis in trastuzumab-resistant HER2-positive tumor tissues from patients and nudemice.Mechanistically,the cell division cycle 42(CDC42)promoted GLS1 expression in tumor cells by activating nuclear factor kappa-B(NF-κB)p65 and drove GLS1microvesicle secretion through IQmotif-containing GTPase-activating protein 1(IQGAP1).Based on the ABM and in vivo experiments,we confirmed that the combination of anti-glutamine metabolism,anti-angiogenesis,and pro-M1 polarization therapy had the best effect in reversing trastuzumab resistance in HER2-positive gastric cancer.Conclusions:This study revealed that tumor cells secrete GLS1 microvesicles via CDC42 to promote glutamine metabolism,M2 macrophage polarization,and pro-angiogenic function of macrophages,leading to acquired trastuzumab resistance in HER2-positive gastric cancer.A combination of anti-glutamine metabolism,anti-angiogenesis,and pro-M1 polarization therapy may provide a new insight into reversing trastuzumab resistance. | Xingbin Hu Zhenfeng Ma Beibei Xu Shulong Li Zhiqi Yao Bishan Liang Jiao Wang Wangjun Liao Li Lin Chunling Wang Siting Zheng Qijing Wu Qiong Huang Le Yu Fenghua Wang Min Shi | 2023 | Cancer Communications2023，43，8： | 0 |
| 14 | Bioinformatics exploration of potential common therapeutic targets for systemic and pulmonary arterial hypertension-induced myocardial hypertrophy显示文摘Systemic and pulmonary arterial hypertension(PAH)can induce left and right ventricular hypertrophy,respectively,but common therapeutic targets for both left and right hypertrophy are limited.In this study,we attempt to explore potential common therapeutic targets and screen out potential target drugs for further study.Cardiac mRNA expression profiles in mice with transverse aortic constriction(TAC)and pulmonary arterial constriction(PAC)are obtained from online databases.After bioinformatics analyses,we generate TAC and PAC mouse models to validate the phenotypes of cardiac remodelling as well as the identified hub genes.Bioinformatics analyses show that there are 214 independent differentially expressed genes(DEGs)in GSE136308(TAC related)and 2607 independent DEGs in GSE30922(PAC related),while 547 shared DEGs are associated with the function of the extracellular matrix(ECM)or involved in the PI3K-Akt signaling pathway,cytokine-cytokine receptor interactions,and ECM-receptor interactions.We identifyd Fn1,Il6,Col1a1,Igf1,Col1a2,Timp1,Col3a1,Cd44,Ctgf and Postn as hub genes of the shared DEGs,and most of them are associated with myocardial fibrosis.Those hub genes and phenotypes of cardiac remodelling are validated in our TAC and PAC mouse models.Furthermore,we identify dehydroisoandrosterone(DHEA),iloprost and 4,5-dianilinophthalimide(DAPH)as potential therapeutic drugs targeting both left and right ventricular hypertrophy and validate the effect of DHEA.These findings suggest that DHEA could be an effective drug for pressure overload-induced left or right ventricular hypertrophy by regulating the shared hub differentially expressed genes associated with fibrosis. | Lu Chen Mingjue Li Mengjia Shen Yingqi Zhu Kaitong Chen Xiaoxia Huang Cankun Zheng Qiancheng Wang Hairuo Lin Wangjun Liao Jianping Bin Siyuan Ma Yulin Liao | 2023 | Acta Biochimica et Biophysica Sinica2023，55，5： | 0 |
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