Cancer and Metastasis Reviews最新文献_第9页

Molecular profile of metastasis, cell plasticity and EMT in pancreatic cancer: a pre-clinical connection to aggressiveness and drug resistance. 胰腺癌转移、细胞可塑性和 EMT 的分子特征：与侵袭性和耐药性的临床前联系。

IF 9.2 2区医学

Cancer and Metastasis Reviews Pub Date : 2024-03-01 Epub Date: 2023-07-15 DOI: 10.1007/s10555-023-10125-y

Zhenli Guo, Milad Ashrafizadeh, Wei Zhang, Rongjun Zou, Gautam Sethi, Xianbin Zhang

{"title":"Molecular profile of metastasis, cell plasticity and EMT in pancreatic cancer: a pre-clinical connection to aggressiveness and drug resistance.","authors":"Zhenli Guo, Milad Ashrafizadeh, Wei Zhang, Rongjun Zou, Gautam Sethi, Xianbin Zhang","doi":"10.1007/s10555-023-10125-y","DOIUrl":"10.1007/s10555-023-10125-y","url":null,"abstract":"The metastasis is a multistep process in which a small proportion of cancer cells are detached from the colony to enter into blood cells for obtaining a new place for metastasis and proliferation. The metastasis and cell plasticity are considered major causes of cancer-related deaths since they improve the malignancy of cancer cells and provide poor prognosis for patients. Furthermore, enhancement in the aggressiveness of cancer cells has been related to the development of drug resistance. Metastasis of pancreatic cancer (PC) cells has been considered one of the major causes of death in patients and their undesirable prognosis. PC is among the most malignant tumors of the gastrointestinal tract and in addition to lifestyle, smoking, and other factors, genomic changes play a key role in its progression. The stimulation of EMT in PC cells occurs as a result of changes in molecular interaction, and in addition to increasing metastasis, EMT participates in the development of chemoresistance. The epithelial, mesenchymal, and acinar cell plasticity can occur and determines the progression of PC. The major molecular pathways including STAT3, PTEN, PI3K/Akt, and Wnt participate in regulating the metastasis of PC cells. The communication in tumor microenvironment can provide by exosomes in determining PC metastasis. The components of tumor microenvironment including macrophages, neutrophils, and cancer-associated fibroblasts can modulate PC progression and the response of cancer cells to chemotherapy.","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"29-53"},"PeriodicalIF":9.2,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9834917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epithelial-to-mesenchymal transition in cancer progression: unraveling the immunosuppressive module driving therapy resistance. 癌症进展中的上皮-间充质转变：揭示驱动治疗耐药性的免疫抑制模块。

IF 9.2 2区医学

Cancer and Metastasis Reviews Pub Date : 2024-03-01 Epub Date: 2023-09-30 DOI: 10.1007/s10555-023-10141-y

Deepti Singh, Hifzur R Siddique

{"title":"Epithelial-to-mesenchymal transition in cancer progression: unraveling the immunosuppressive module driving therapy resistance.","authors":"Deepti Singh, Hifzur R Siddique","doi":"10.1007/s10555-023-10141-y","DOIUrl":"10.1007/s10555-023-10141-y","url":null,"abstract":"Cancer cells undergo phenotypic switching (cancer cell plasticity) in response to microenvironmental cues, including exposure to therapy/treatment. Phenotypic plasticity enables the cancer cells to acquire more mesenchymal traits promoting cancer cells' growth, survival, therapy resistance, and disease recurrence. A significant program in cancer cell plasticity is epithelial-to-mesenchymal transition (EMT), wherein a comprehensive reprogramming of gene expression occurs to facilitate the translational shift from epithelial-to-mesenchymal phenotypes resulting in increased invasiveness and metastasis. In addition, EMT plays a pivotal role in facilitating cancer cells' escape from the body's immune system using several mechanisms, such as the downregulation of major histocompatibility complex-mediated antigen presentation, upregulation of immune checkpoint molecules, and recruitment of immune-suppressive cells. Cancer cells' ability to undergo phenotypic switching and EMT-driven immune escape presents a formidable obstacle in cancer management, highlighting the need to unravel the intricate mechanisms underlying these processes and develop novel therapeutic strategies. This article discusses the role of EMT in promoting immune evasion and therapy resistance. We also discuss the ongoing research on developing therapeutic approaches targeting intrinsic and induced cell plasticity within the immune suppressive microenvironment. We believe this review article will update the current research status and equip researchers, clinicians, and other healthcare professionals with valuable insights enhancing their existing knowledge and shedding light on promising directions for future cancer research. This will facilitate the development of innovative strategies for managing therapy-resistant cancers and improving patient outcomes.","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"155-173"},"PeriodicalIF":9.2,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41105523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Biographies. 传记

IF 9.2 2区医学

Cancer and Metastasis Reviews Pub Date : 2024-03-01 DOI: 10.1007/s10555-024-10179-6

引用次数: 0

Harnessing function of EMT in cancer drug resistance: a metastasis regulator determines chemotherapy response. 利用 EMT 在癌症耐药性中的功能：转移调节器决定化疗反应。

IF 9.2 2区医学

Cancer and Metastasis Reviews Pub Date : 2024-03-01 Epub Date: 2024-01-16 DOI: 10.1007/s10555-023-10162-7

Nasim Ebrahimi, Mahdokht Sadat Manavi, Ferdos Faghihkhorasani, Siavash Seifollahy Fakhr, Fatemeh Jafari Baei, Fereshteh Faghih Khorasani, Mohammad Mehdi Zare, Nazanin Pazhouhesh Far, Fatemeh Rezaei-Tazangi, Jun Ren, Russel J Reiter, Noushin Nabavi, Amir Reza Aref, Chu Chen, Yavuz Nuri Ertas, Qi Lu

{"title":"Harnessing function of EMT in cancer drug resistance: a metastasis regulator determines chemotherapy response.","authors":"Nasim Ebrahimi, Mahdokht Sadat Manavi, Ferdos Faghihkhorasani, Siavash Seifollahy Fakhr, Fatemeh Jafari Baei, Fereshteh Faghih Khorasani, Mohammad Mehdi Zare, Nazanin Pazhouhesh Far, Fatemeh Rezaei-Tazangi, Jun Ren, Russel J Reiter, Noushin Nabavi, Amir Reza Aref, Chu Chen, Yavuz Nuri Ertas, Qi Lu","doi":"10.1007/s10555-023-10162-7","DOIUrl":"10.1007/s10555-023-10162-7","url":null,"abstract":"Epithelial-mesenchymal transition (EMT) is a complicated molecular process that governs cellular shape and function changes throughout tissue development and embryogenesis. In addition, EMT contributes to the development and spread of tumors. Expanding and degrading the surrounding microenvironment, cells undergoing EMT move away from the main location. On the basis of the expression of fibroblast-specific protein-1 (FSP1), fibroblast growth factor (FGF), collagen, and smooth muscle actin (-SMA), the mesenchymal phenotype exhibited in fibroblasts is crucial for promoting EMT. While EMT is not entirely reliant on its regulators like ZEB1/2, Twist, and Snail proteins, investigation of upstream signaling (like EGF, TGF-β, Wnt) is required to get a more thorough understanding of tumor EMT. Throughout numerous cancers, connections between tumor epithelial and fibroblast cells that influence tumor growth have been found. The significance of cellular crosstalk stems from the fact that these events affect therapeutic response and disease prognosis. This study examines how classical EMT signals emanating from various cancer cells interfere to tumor metastasis, treatment resistance, and tumor recurrence.","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"457-479"},"PeriodicalIF":9.2,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139472299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Preface. 序言

IF 9.2 2区医学

Cancer and Metastasis Reviews Pub Date : 2024-03-01 DOI: 10.1007/s10555-024-10180-z

Hifzur R Siddique, Ajaikumar B Kunnumakkara

引用次数: 0

From modulation of cellular plasticity to potentiation of therapeutic resistance: new and emerging roles of MYB transcription factors in human malignancies. 从细胞可塑性的调节到治疗耐药性的增强：MYB转录因子在人类恶性肿瘤中的新作用。

IF 9.2 2区医学

Cancer and Metastasis Reviews Pub Date : 2024-03-01 Epub Date: 2023-11-10 DOI: 10.1007/s10555-023-10153-8

Shashi Anand, Kunwar Somesh Vikramdeo, Sarabjeet Kour Sudan, Amod Sharma, Srijan Acharya, Mohammad Aslam Khan, Seema Singh, Ajay Pratap Singh

{"title":"From modulation of cellular plasticity to potentiation of therapeutic resistance: new and emerging roles of MYB transcription factors in human malignancies.","authors":"Shashi Anand, Kunwar Somesh Vikramdeo, Sarabjeet Kour Sudan, Amod Sharma, Srijan Acharya, Mohammad Aslam Khan, Seema Singh, Ajay Pratap Singh","doi":"10.1007/s10555-023-10153-8","DOIUrl":"10.1007/s10555-023-10153-8","url":null,"abstract":"MYB transcription factors are encoded by a large family of highly conserved genes from plants to vertebrates. There are three members of the MYB gene family in human, namely, MYB, MYBL1, and MYBL2 that encode MYB/c-MYB, MYBL1/A-MYB, and MYBL2/B-MYB, respectively. MYB was the first member to be identified as a cellular homolog of the v-myb oncogene carried by the avian myeloblastosis virus (AMV) causing leukemia in chickens. Under the normal scenario, MYB is predominantly expressed in hematopoietic tissues, colonic crypts, and neural stem cells and plays a role in maintaining the undifferentiated state of the cells. Over the years, aberrant expression of MYB genes has been reported in several malignancies and recent years have witnessed tremendous progress in understanding of their roles in processes associated with cancer development. Here, we review various MYB alterations reported in cancer along with the roles of MYB family proteins in tumor cell plasticity, therapy resistance, and other hallmarks of cancer. We also discuss studies that provide mechanistic insights into the oncogenic functions of MYB transcription factors to identify potential therapeutic vulnerabilities.","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"409-421"},"PeriodicalIF":9.2,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11015973/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72208460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The emerging role of the gut microbiome in cancer cell plasticity and therapeutic resistance. 肠道微生物组在癌细胞可塑性和抗药性中的新作用。

IF 9.2 2区医学

Cancer and Metastasis Reviews Pub Date : 2024-03-01 Epub Date: 2023-09-14 DOI: 10.1007/s10555-023-10138-7

Priya Mondal, Syed Musthapa Meeran

{"title":"The emerging role of the gut microbiome in cancer cell plasticity and therapeutic resistance.","authors":"Priya Mondal, Syed Musthapa Meeran","doi":"10.1007/s10555-023-10138-7","DOIUrl":"10.1007/s10555-023-10138-7","url":null,"abstract":"Resistance to therapeutic agents is one of the major challenges in cancer therapy. Generally, the focus is given to the genetic driver, especially the genetic mutation behind the therapeutic resistance. However, non-mutational mechanisms, such as epigenetic modifications, and TME alteration, which is mainly driven by cancer cell plasticity, are also involved in therapeutic resistance. The concept of plasticity mainly relies on the conversion of non-cancer stem cells (CSCs) to CSCs or epithelial-to-mesenchymal transition via different mechanisms and various signaling pathways. Cancer plasticity plays a crucial role in therapeutic resistance as cancer cells are able to escape from therapeutics by shifting the phenotype and thereby enhancing tumor progression. New evidence suggests that gut microbiota can change cancer cell characteristics by impacting the mechanisms involved in cancer plasticity. Interestingly, gut microbiota can also influence the therapeutic efficacy of anticancer drugs by modulating the mechanisms involved in cancer cell plasticity. The gut microbiota has been shown to reduce the toxicity of certain clinical drugs. Here, we have documented the critical role of the gut microbiota on the therapeutic efficacy of existing anticancer drugs by altering the cancer plasticity. Hence, the extended knowledge of the emerging role of gut microbiota in cancer cell plasticity can help to develop gut microbiota-based novel therapeutics to overcome the resistance or reduce the toxicity of existing drugs. Furthermore, to improve the effectiveness of therapy, it is necessary to conduct more clinical and preclinical research to fully comprehend the mechanisms of gut microbiota.","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"135-154"},"PeriodicalIF":9.2,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10234974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sam68 is a druggable vulnerability point in cancer stem cells. Sam68是癌症干细胞中的一个药物脆弱点。

IF 9.2 2区医学

Cancer and Metastasis Reviews Pub Date : 2024-03-01 Epub Date: 2023-10-04 DOI: 10.1007/s10555-023-10145-8

Amanda Mendes da Silva, Veronika Yevdokimova, Yannick D Benoit

{"title":"Sam68 is a druggable vulnerability point in cancer stem cells.","authors":"Amanda Mendes da Silva, Veronika Yevdokimova, Yannick D Benoit","doi":"10.1007/s10555-023-10145-8","DOIUrl":"10.1007/s10555-023-10145-8","url":null,"abstract":"Sam68 (Src associated in mitosis of 68 kDa) is an RNA-binding and multifunctional protein extensively characterized in numerous cellular functions, such as RNA processing, cell cycle regulation, kinase- and growth factor signaling. Recent investigations highlighted Sam68 as a primary target of a class of reverse-turn peptidomimetic drugs, initially developed as inhibitors of Wnt/β-catenin mediated transcription. Further investigations on such compounds revealed their capacity to selectively eliminate cancer stem cell (CSC) activity upon engaging Sam68. This work highlighted previously unappreciated roles for Sam68 in the maintenance of neoplastic self-renewal and tumor-initiating functions. Here, we discuss the implication of Sam68 in tumorigenesis, where central findings support its contribution to chromatin regulation processes essential to CSCs. We also review advances in CSC-targeting drug discovery aiming to modulate Sam68 cellular distribution and protein-protein interactions. Ultimately, Sam68 constitutes a vulnerability point of CSCs and an attractive therapeutic target to impede neoplastic stemness in human tumors.","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"441-456"},"PeriodicalIF":9.2,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11016129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41101432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dynamic interplay of nuclear receptors in tumor cell plasticity and drug resistance: Shifting gears in malignant transformations and applications in cancer therapeutics. 核受体在肿瘤细胞可塑性和耐药性中的动态相互作用：恶性转变中的换挡以及在癌症治疗中的应用。

IF 9.2 2区医学

Cancer and Metastasis Reviews Pub Date : 2024-03-01 Epub Date: 2024-03-22 DOI: 10.1007/s10555-024-10171-0

Bandari BharathwajChetty, Anjana Sajeev, Ravichandran Vishwa, Babu Santha Aswani, Mohammed S Alqahtani, Mohamed Abbas, Ajaikumar B Kunnumakkara

{"title":"Dynamic interplay of nuclear receptors in tumor cell plasticity and drug resistance: Shifting gears in malignant transformations and applications in cancer therapeutics.","authors":"Bandari BharathwajChetty, Anjana Sajeev, Ravichandran Vishwa, Babu Santha Aswani, Mohammed S Alqahtani, Mohamed Abbas, Ajaikumar B Kunnumakkara","doi":"10.1007/s10555-024-10171-0","DOIUrl":"10.1007/s10555-024-10171-0","url":null,"abstract":"Recent advances have brought forth the complex interplay between tumor cell plasticity and its consequential impact on drug resistance and tumor recurrence, both of which are critical determinants of neoplastic progression and therapeutic efficacy. Various forms of tumor cell plasticity, instrumental in facilitating neoplastic cells to develop drug resistance, include epithelial-mesenchymal transition (EMT) alternatively termed epithelial-mesenchymal plasticity, the acquisition of cancer stem cell (CSC) attributes, and transdifferentiation into diverse cell lineages. Nuclear receptors (NRs) are a superfamily of transcription factors (TFs) that play an essential role in regulating a multitude of cellular processes, including cell proliferation, differentiation, and apoptosis. NRs have been implicated to play a critical role in modulating gene expression associated with tumor cell plasticity and drug resistance. This review aims to provide a comprehensive overview of the current understanding of how NRs regulate these key aspects of cancer biology. We discuss the diverse mechanisms through which NRs influence tumor cell plasticity, including EMT, stemness, and metastasis. Further, we explore the intricate relationship between NRs and drug resistance, highlighting the impact of NR signaling on chemotherapy, radiotherapy and targeted therapies. We also discuss the emerging therapeutic strategies targeting NRs to overcome tumor cell plasticity and drug resistance. This review also provides valuable insights into the current clinical trials that involve agonists or antagonists of NRs modulating various aspects of tumor cell plasticity, thereby delineating the potential of NRs as therapeutic targets for improved cancer treatment outcomes.","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"321-362"},"PeriodicalIF":9.2,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140189419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lipid metabolism and its implications in tumor cell plasticity and drug resistance: what we learned thus far? 脂质代谢及其对肿瘤细胞可塑性和耐药性的影响：迄今为止我们学到了什么？

IF 9.2 2区医学

Cancer and Metastasis Reviews Pub Date : 2024-03-01 Epub Date: 2024-03-05 DOI: 10.1007/s10555-024-10170-1

Ravichandran Vishwa, Bandari BharathwajChetty, Sosmitha Girisa, Babu Santha Aswani, Mohammed S Alqahtani, Mohamed Abbas, Mangala Hegde, Ajaikumar B Kunnumakkara

{"title":"Lipid metabolism and its implications in tumor cell plasticity and drug resistance: what we learned thus far?","authors":"Ravichandran Vishwa, Bandari BharathwajChetty, Sosmitha Girisa, Babu Santha Aswani, Mohammed S Alqahtani, Mohamed Abbas, Mangala Hegde, Ajaikumar B Kunnumakkara","doi":"10.1007/s10555-024-10170-1","DOIUrl":"10.1007/s10555-024-10170-1","url":null,"abstract":"Metabolic reprogramming, a hallmark of cancer, allows cancer cells to adapt to their specific energy needs. The Warburg effect benefits cancer cells in both hypoxic and normoxic conditions and is a well-studied reprogramming of metabolism in cancer. Interestingly, the alteration of other metabolic pathways, especially lipid metabolism has also grabbed the attention of scientists worldwide. Lipids, primarily consisting of fatty acids, phospholipids and cholesterol, play essential roles as structural component of cell membrane, signalling molecule and energy reserves. This reprogramming primarily involves aberrations in the uptake, synthesis and breakdown of lipids, thereby contributing to the survival, proliferation, invasion, migration and metastasis of cancer cells. The development of resistance to the existing treatment modalities poses a major challenge in the field of cancer therapy. Also, the plasticity of tumor cells was reported to be a contributing factor for the development of resistance. A number of studies implicated that dysregulated lipid metabolism contributes to tumor cell plasticity and associated drug resistance. Therefore, it is important to understand the intricate reprogramming of lipid metabolism in cancer cells. In this review, we mainly focused on the implication of disturbed lipid metabolic events on inducing tumor cell plasticity-mediated drug resistance. In addition, we also discussed the concept of lipid peroxidation and its crucial role in phenotypic switching and resistance to ferroptosis in cancer cells. Elucidating the relationship between lipid metabolism, tumor cell plasticity and emergence of resistance will open new opportunities to develop innovative strategies and combinatorial approaches for the treatment of cancer.","PeriodicalId":9489,"journal":{"name":"Cancer and Metastasis Reviews","volume":" ","pages":"293-319"},"PeriodicalIF":9.2,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140027438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0