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Tumor microenvironment involvement in colorectal cancer progression via Wnt/β-catenin pathway:Providing understanding of the complex mechanisms of chemoresistance

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World Journal of Gastroenterology 2022年第26期28卷 3027-3046页

作者： María Belén Novoa Díaz María Julia Martín Claudia Gentili Departamento de Biología Bioquímica y FarmaciaUniversidad Nacional del Sur(UNS)-INBIOSUR(CONICET-UNS)Bahía Blanca 8000Argentina Departamento de Química Universidad Nacional del Sur(UNS)-INQUISUR(CONICET-UNS)Bahía Blanca 8000Argentina

Colorectal cancer(CRC)continues to be one of the main causes of death from cancer because patients progress unfavorably due to resistance to current therapies.Dysregulation of the Wnt/β-catenin pathway plays a fundamental role in the genesis and progression of several types of cancer,including CRC.In many subtypes of CRC,hyperactivation of theβ-catenin pathway is associated with mutations of the adenomatous polyposis coli gene.However,it can also be associated with other causes.In recent years,studies of the tumor microenvironment(TME)have demonstrated its importance in the development and progression of CRC.In this tumor nest,several cell types,structures,and biomolecules interact with neoplastic cells to pave the way for the spread of the disease.Cross-communications between tumor cells and the TME are then established primarily through paracrine factors,which trigger the activation of numerous signaling pathways.Crucial advances in the field of oncology have been made in the last decade.This Minireview aims to actualize what is known about the central role of the Wnt/β-catenin pathway in CRC chemoresistance and aggressiveness,focusing on crosscommunication between CRC cells and the TME.Through this analysis,our main objective was to increase the understanding of this complex disease considering a more global context.Since many treatments for advanced CRC fail due to mechanisms involving chemoresistance,the data here exposed and analyzed are of great interest for the development of novel and effective therapies.

关键词： Colorectal cancer β-catenin pathway Tumor stroma Tumor microenvironment factors cancer progression Drug resistance

Extracellular matrix in cancer progression and therapy

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Medical Review 2022年第2期2卷 125-139页

作者： Xiuxiu He Byoungkoo Lee Yi Jiang Department of Medical Physics Memorial Sloan-Kettering Cancer CenterNew YorkNYUSA The Jackson Laboratory for Genomic Medicine FarmingtonCTUSA Department of Mathematics and Statistics Georgia State University25 Park PlaceAtlantaGA 30303USA

The tumor ecosystem with heterogeneous cellularcompositions and the tumor microenvironment has increasingly become the focus of cancer research in recent years. Theextracellular matrix (ECM), the major component of the tumor microenvironment, and its interactions with the tumorcells and stromal cells have also enjoyed tremendouslyincreased attention. Like the other components of the tumormicroenvironment, the ECM in solid tumors differs significantly from that in normal organs and tissues. We reviewrecent studies of the complex roles the tumor ECM plays incancer progression, from tumor initiation, growth to angiogenesis and invasion. We highlight that the biomolecular,biophysical, and mechanochemical interactions between theECM and cells not only regulate the steps of cancer progression, but also affect the efficacy of systemic cancer treatment.We further discuss the strategies to target and modify thetumor ECM to improve cancer therapy.

关键词： cancer invasion cancer metabolism cancer progression cancer therapy cell-ECM interaction extracellular matrix metastasis

Silencing of the long non-coding RNA LINC00265 triggers autophagy and apoptosis in lung cancer by reducing protein stability of SIN3A oncogene

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Oncology Research 2024年第7期32卷 1185-1195页

作者： XIAOBI HUANG CHUNYUAN CHEN YONGYANG CHEN HONGLIAN ZHOU YONGHUA CHEN ZHONG HUANG YULIU XIE BAIYANG LIU YUDONG GUO ZHIXIONG YANG GUANGHUA CHEN WENMEI SU Department of Pulmonary Oncology Affiliated Hospital of Guangdong Medical UniversityZhanjiang524001China Department of Thoracic Surgery Affiliated Hospital of Guangdong Medical UniversityZhanjiang524001China Department of Orthopedics Affiliated Hospital of Guangdong Medical UniversityZhanjiang524001China Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases Affiliated Hospital of Guangdong Medical UniversityZhanjiang524001China

Background:Long non-coding RNAs are important regulators in cancer biology and function either as tumor suppressors or as oncogenes.Their dysregulation has been closely associated with tumorigenesis.LINC00265 is upregulated in lung adenocarcinoma and is a prognostic biomarker of this cancer.However,the mechanism underlying its function in cancer progression remains poorly understood.Methods:Here,the regulatory role of LINC00265 in lung adenocarcinoma was examined using lung cancer cell lines,clinical samples,and xenografts.Results:We found that high levels of LINC00265 expression were associated with shorter overall survival rate of patients,whereas knockdown of LINC00265 inhibited proliferation of cancer cell lines and tumor growth in xenografts.Western blot andﬂow cytometry analyses indicated that silencing of LINC00265 induced autophagy and apoptosis.Moreover,we showed that LINC00265 interacted with and stabilized the transcriptional co-repressor Switch-independent 3a(SIN3A),which is a scaffold protein functioning either as a tumor repressor or as an oncogene in a context-dependent manner.Silencing of SIN3A also reduced proliferation of lung cancer cells,which was correlated with the induction of autophagy.These observations raise the possibility that LINC00265 functions to promote the oncogenic activity of SIN3A in lung adenocarcinoma.Conclusions:Ourﬁndings thus identify SIN3A as a LINC00265-associated protein and should help to understand the mechanism underlying LINC00265-mediated oncogenesis.

关键词： LINC00265 Autophagy Lung adenocarcinoma(LUAD) cancer progression Switch-independent 3a(SIN3A)

Multifaceted roles and functions of SOX30 in human cancer

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cancer Innovation 2024年第2期3卷 11-27页

作者： Na Sun Cheng Wang Pingping Gao Rui Wang Yi Zhang Xiaowei Qi Department of Breast and Thyroid Surgery The Southwest Hospital of Army Medical UniversityChongqingChina

SRY-box transcription factor 30(SOX30)participates in tumor cell apoptosis in lung cancer.The occurrence of somatic SOX30 mutations,the expression signature of SOX30 in normal and cancer tissues,the correlation of SOX30 with immune cells and immune-related genes,and the clinical significance of SOX30 in various cancers have stimulated interest in SOX30 as a potential cancer biomarker.SOX30 influences drug sensitivity and tumor immunity in specific cancer types.In this review,we have comprehensively summarized the latest research on the role of SOX30 in cancer by combining bioinformatics evidence and a literature review.We summarize recent research on SOX30 in cancer regarding somatic mutations,trials,transcriptome analysis,clinical information,and SOX30-mediated regulation of malignant phenotypes.Additionally,we report on the diagnostic value of SOX30 mRNA expression levels across different cancer types.This review on the role of SOX30 in cancer progression may provide insights into possible research directions for SOX30 in cancer and a theoretical basis for guiding future studies.

关键词： cancer progression prognosis SOX30

Role of doublecortin-like kinase 1 and leucine-rich repeat-containing G-protein-coupled receptor 5 in patients with stage Ⅱ/Ⅲ colorectal cancer:cancer progression and prognosis

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World Journal of Gastroenterology 2020年第43期26卷 6853-6866页

作者： Xue-Ling Kang Li-Rui He Yao-Li Chen Shu-Bin Wang Department of Oncology Peking University Shenzhen HospitalShenzhen-Peking University-Hong Kong University of Science and Technology Medical CenterShenzhen 518036Guangdong ProvinceChina Department of Gastrointestinal Surgery Peking University Shenzhen HospitalShenzhen 518036Guangdong ProvinceChina Department of Pathology Peking University Shenzhen HospitalShenzhen 518036Guangdong ProvinceChina Department of Oncology Peking University Shenzhen HospitalShenzhen Key Laboratory of Gastrointestinal Cancer Translational ResearchChina Cancer Institute of Shenzhen-Peking University-Hong Kong University of Science and Technology Medical CenterShenzhen 518036Guangdong ProvinceChina

BACKGROUND cancer stem cells(CSCs)are a subpopulation of cancer cells with the potential of self-renewal and differentiation.CSCs play critical roles in tumorigenesis,recurrence,metastasis,radiation tolerance and chemoresistance.AIM To assess the expression patterns and clinical potential of doublecortin-like kinase 1(DCLK1)and leucine-rich repeat-containing G-protein-coupled receptor 5(Lgr5),as prognostic CSC markers of colorectal cancer(CRC).METHODS The expression of DCLK1 and Lgr5 in CRC tissue sections from 92 patients was determined by immunohistochemistry.Each case was evaluated using a combined scoring method based on signal intensity staining(scored 0-3)and the proportion of positively stained cancer cells(scored 0-3).The final staining score was calculated as the intensity score multiplied by the proportion score.Low expression of DCLK1 and Lgr5 was defined as a score of 0-3;high expression of DCLK1 and Lgr5 was defined as a score of≥4.Specimens were categorized as either high or low expression,and the correlation between the expression of DCLK1 or Lgr5 and clinicopathological factors was investigated.RESULTS DCLK1 and Lgr5 expression levels were significantly positively correlated.CRC patients with high DCLK1,Lgr5 and DCLK1/Lgr5 expressions had poorer progression-free survival and overall survival.Moreover,high expression of DCLK1 was an independent prognostic factor for recurrence and overall survival in patients with CRC by multivariate analysis(P=0.026 and P=0.049,respectively).CONCLUSION DCLK1 may be a potential CSC marker for the recurrence and survival of CRC patients.

关键词： Colorectal cancer cancer stem cells Doublecortin-like kinase 1 Leucine-rich repeat-containing G-protein-coupled receptor 5 cancer prognosis cancer progression

The regulatory and modulatory roles of TRP family channels in malignant tumors and relevant therapeutic strategies

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Acta Pharmaceutica Sinica B 2022年第4期12卷 1761-1780页

作者： Tiecheng Zhong Wenxin Zhang Hongjie Guo Xiaohui Pan Xi Chen Qiaojun He Bo Yang Ling Ding Zhejiang Province Key Laboratory of Anti-cancer Drug Research Institute of Pharmacology and ToxicologyCollege of Pharmaceutical SciencesZhejiang UniversityHangzhou 310058China

Transient receptor potential(TRP)channels are one primary type of calcium(Ca^(2+))permeable channels,and those relevant transmembrane and intracellular TRP channels were previously thought to be mainly associated with the regulation of cardiovascular and neuronal systems.Nowadays,however,accumulating evidence shows that those TRP channels are also responsible for tumorigenesis and progression,inducing tumor invasion and metastasis.However,the overall underlying mechanisms and possible signaling transduction pathways that TRP channels in malignant tumors might still remain elusive.Therefore,in this review,we focus on the linkage between TRP channels and the significant characteristics of tumors such as multi-drug resistance(MDR),metastasis,apoptosis,proliferation,immune surveillance evasion,and the alterations of relevant tumor micro-environment.Moreover,we also have discussed the expression of relevant TRP channels in various forms of cancer and the relevant inhibitors’efficacy.The chemo-sensitivity of the anti-cancer drugs of various acting mechanisms and the potential clinical applications are also presented.Furthermore,it would be enlightening to provide possible novel therapeutic approaches to counteract malignant tumors regarding the intervention of calcium channels of this type.

关键词： TRP channels cancer progression Tumor microenvironment Tumor-associated immunocytes Intracellular mechanism Programmed cancer cell death Targeted tumor therapy

How the interplay among the tumor microenvironment and the gut microbiota influences the stemness of colorectal cancer cells

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World Journal of Stem Cells 2023年第5期15卷 281-301页

作者： María Belén Novoa Díaz Pedro Carriere Claudia Gentili Departamento de Biología Bioquímica y FarmaciaUniversidad Nacional del SurBahía Blanca 8000Buenos AiresArgentina Instituto de Ciencias Biológicas y Biomédicas del Sur Consejo Nacional de Investigaciones Científicas y Técnicas(CONICET)-Universidad Nacional del Sur(UNS)Bahía Blanca 8000Buenos AiresArgentina

Colorectal cancer(CRC)remains the third most prevalent cancer disease and involves a multi-step process in which intestinal cells acquire malignant characteristics.It is well established that the appearance of distal metastasis in CRC patients is the cause of a poor prognosis and treatment failure.Nevertheless,in the last decades,CRC aggressiveness and progression have been attributed to a specific cell population called CRC stem cells(CCSC)with features like tumor initiation capacity,self-renewal capacity,and acquired multidrug resistance.Emerging data highlight the concept of this cell subtype as a plastic entity that has a dynamic status and can be originated from different types of cells through genetic and epigenetic changes.These alterations are modulated by complex and dynamic crosstalk with environmental factors by paracrine signaling.It is known that in the tumor niche,different cell types,structures,and biomolecules coexist and interact with cancer cells favoring cancer growth and development.Together,these components constitute the tumor microenvironment(TME).Most recently,researchers have also deepened the influence of the complex variety of microorganisms that inhabit the intestinal mucosa,collectively known as gut microbiota,on CRC.Both TME and microorganisms participate in inflammatory processes that can drive the initiation and evolution of CRC.Since in the last decade,crucial advances have been made concerning to the synergistic interaction among the TME and gut microorganisms that condition the identity of CCSC,the data exposed in this review could provide valuable insights into the biology of CRC and the development of new targeted therapies.

关键词： Colorectal cancer Colorectal cancer stem cells Tumor microenvironment factors Tumor stroma Gut microbiota cancer progression

Function of cancer cell-derived extracellular matrix in tumor progression

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Journal of cancer Metastasis and Treatment 2016年第1期2卷 357-364页

作者： Gao-Feng Xiong Ren Xu Markey cancer Center LexingtonKY 40536USA Department of Pharmacology and Nutritional Sciences University of KentuckyLexingtonKY 40536USA

Extracellular matrix(ECM)is an essential component of the tumor microenvironment.cancer development and progression are associated with increased ECM deposition and crosslink.The chemical and physical signals elicited from ECM are necessary for cancer cell proliferation and invasion.It is well recognized that stromal cells are a major source of ECM proteins.However,recent studies showed that cancer cells are also an active and important component in ECM remodeling.cancer cells deposit a significant amount of collagen,fibronectin,and tenascin C(TNC).Recent studies demonstrate that these cancer cell-derived ECM proteins enhance cancer cell survival and promote cancer cell colonization at distant sites.ECM-related enzymes and chaperone proteins,such as prolyl-4-hydroxylase,lysyl-hydroxylase,lysyl oxidase,and heat shock protein 47,are also highly expressed in cancer cells.Inhibition of these enzymes significantly reduces cancer growth,invasion,and metastasis.These factors suggest that the cancer cell-derived ECM is crucial for cancer progression and metastasis.Therefore,targeting these ECM proteins and ECM-related enzymes is a potential strategy for cancer treatment.

关键词： Tumor microenvironment extracellular matrix cancer progression metastasis

Monoacylglycerol lipase regulates cannabinoid receptor 2-dependent macrophage activation and cancer progression

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Monoacylglycerol lipase regulates cannabinoid receptor 2-dep...