Cancer growth and metastasis最新文献

Apoptosis-Induced Compensatory Proliferation in Cancer 肿瘤细胞凋亡诱导的代偿性增殖

Cancer growth and metastasis Pub Date : 2021-11-25 DOI: 10.36255/exon-publications.metastasis.apoptosis-proliferation

Ulisses Moreno-Celis, T. García-Gasca, C. Mejía

{"title":"Apoptosis-Induced Compensatory Proliferation in Cancer","authors":"Ulisses Moreno-Celis, T. García-Gasca, C. Mejía","doi":"10.36255/exon-publications.metastasis.apoptosis-proliferation","DOIUrl":"https://doi.org/10.36255/exon-publications.metastasis.apoptosis-proliferation","url":null,"abstract":"Apoptosis is a biological process that allows adequate cellular turnover and the elimination of damaged or infected cells. However, there are compensatory molecular mechanisms that promote cell proliferation after increased apoptotic events. These events are commonly mediated by mitogenic proteins, released by apoptotic cells, and received by neighboring cells, that trigger mechanisms similar to cell repair after an injury or traumatic event. This Note to the Reader: This chapter is part of the book Metastasis (ISBN: 978-0-6453320-2-5), scheduled for publication in April 2022. The book is being published by Exon Publications , Brisbane, Australia, and edited by Professor Consolato M. Segi, MD, PhD, MPH, FRCPC, FCAP, Anatomic Pathology Division, Children's Hospital of Eastern Ontario, ON, Canada. This chapter was published under the Rapid Publication service. It effect is known as \"apoptosis-induced proliferation\". This chapter addresses the process of apoptosis-induced proliferation, the regulatory mechanisms, and its importance in cancer development, progression, and therapy development. protein CCN1 suppresses hepatocarcinogenesis by inhibiting compensatory proliferation. Oncogene.","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"52 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84966917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Metastasis: Methods and Protocols 转移:方法和方案

Cancer growth and metastasis Pub Date : 2021-11-19 DOI: 10.1007/978-1-0716-1350-4

引用次数: 1

Targeting Apoptosis to Overcome Chemotherapy Resistance 靶向细胞凋亡克服化疗耐药

Cancer growth and metastasis Pub Date : 2021-11-19 DOI: 10.36255/exon-publications.metastasis.chemotherapy-resistance

Eda Dogan, H. Kara, B. Kosova, V. Cetintas, Ege

{"title":"Targeting Apoptosis to Overcome Chemotherapy Resistance","authors":"Eda Dogan, H. Kara, B. Kosova, V. Cetintas, Ege","doi":"10.36255/exon-publications.metastasis.chemotherapy-resistance","DOIUrl":"https://doi.org/10.36255/exon-publications.metastasis.chemotherapy-resistance","url":null,"abstract":"Chemotherapy resistance is a major limiting factor for the extensive use of chemotherapeutic drugs in cancer treatment. Despite the large number of newly discovered medications, treatment success rates are still unsatisfactory. Programmed cell death, called apoptosis, is one of the main tissue homeostasis mechanisms that balances cell survival and death. Apoptosis can be induced through extrinsic and intrinsic pathways or repressed by inhibitor proteins. During tumor progression, homeostasis between the anti-apoptotic and pro-apoptotic regulators is disturbed and shifted towards survival through various escape mechanisms. Dysregulation of apoptosis-regulatory mediators, particularly high levels of anti-apoptotic proteins, is one of the main mechanisms by which tumor cells acquire resistance to chemo- and radiotherapy. Therefore, it is important to restore apoptosis in the chemo- and radiotherapy-resistant tumor cells. In this chapter, we summarize general chemotherapy resistance mechanisms, discuss the role of extrinsic and intrinsic pathways in chemoresistance, and review the current experimental strategies to overcome chemotherapy resistance targeting the apoptotic pathways. Note Reader: book April The book","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88744460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

CD133 Promotes Adhesion to the Ovarian Cancer Metastatic Niche. CD133促进卵巢癌转移小生境的粘附。

Cancer growth and metastasis Pub Date : 2018-04-09 eCollection Date: 2018-01-01 DOI: 10.1177/1179064418767882

Lynn Roy, Alexander Bobbs, Rachel Sattler, Jeffrey L Kurkewich, Paige B Dausinas, Prakash Nallathamby, Karen D Cowden Dahl

{"title":"CD133 Promotes Adhesion to the Ovarian Cancer Metastatic Niche.","authors":"Lynn Roy, Alexander Bobbs, Rachel Sattler, Jeffrey L Kurkewich, Paige B Dausinas, Prakash Nallathamby, Karen D Cowden Dahl","doi":"10.1177/1179064418767882","DOIUrl":"https://doi.org/10.1177/1179064418767882","url":null,"abstract":"Cancer stem cells (CSCs) are an attractive therapeutic target due to their predicted role in both metastasis and chemoresistance. One of the most commonly agreed on markers for ovarian CSCs is the cell surface protein CD133. CD133+ ovarian CSCs have increased tumorigenicity, resistance to chemotherapy, and increased metastasis. Therefore, we were interested in defining how CD133 is regulated and whether it has a role in tumor metastasis. Previously we found that overexpression of the transcription factor, ARID3B, increased the expression of PROM1 (CD133 gene) in ovarian cancer cells in vitro and in xenograft tumors. We report that ARID3B directly regulates PROM1 expression. Importantly, in a xenograft mouse model of ovarian cancer, knockdown of PROM1 in cells expressing exogenous ARID3B resulted in increased survival time compared with cells expressing ARID3B and a control short hairpin RNA. This indicated that ARID3B regulation of PROM1 is critical for tumor growth. Moreover, we hypothesized that CD133 may affect metastatic spread. Given that the peritoneal mesothelium is a major site of ovarian cancer metastasis, we explored the role of PROM1 in mesothelial attachment. PROM1 expression increased adhesion to mesothelium in vitro and ex vivo. Collectively, our work demonstrates that ARID3B regulates PROM1 adhesion to the ovarian cancer metastatic niche.","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"11 ","pages":"1179064418767882"},"PeriodicalIF":0.0,"publicationDate":"2018-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179064418767882","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36016339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 32

The Impact of Radiation on the Tumor Microenvironment: Effect of Dose and Fractionation Schedules. 辐射对肿瘤微环境的影响:剂量和分离时间表的影响。

Cancer growth and metastasis Pub Date : 2018-03-09 eCollection Date: 2018-01-01 DOI: 10.1177/1179064418761639

Kimberly M Arnold, Nicole J Flynn, Adam Raben, Lindsay Romak, Yan Yu, Adam P Dicker, Firas Mourtada, Jennifer Sims-Mourtada

引用次数: 105

Inflammation-Generated Extracellular Matrix Fragments Drive Lung Metastasis. 炎症产生的细胞外基质碎片驱动肺转移。

Cancer growth and metastasis Pub Date : 2017-12-21 eCollection Date: 2017-01-01 DOI: 10.1177/1179064417745539

Sandrine Bekaert, Marianne Fillet, Benoit Detry, Muriel Pichavant, Raphael Marée, Agnes Noel, Natacha Rocks, Didier Cataldo

引用次数: 12

Neutrophil-Derived Interleukin 16 in Premetastatic Lungs Promotes Breast Tumor Cell Seeding. 转移前肺部中性粒细胞衍生的白细胞介素 16 可促进乳腺肿瘤细胞播种

Cancer growth and metastasis Pub Date : 2017-10-27 eCollection Date: 2017-01-01 DOI: 10.1177/1179064417738513

Kim Donati, Christelle Sépult, Natacha Rocks, Silvia Blacher, Catherine Gérard, Agnès Noel, Didier Cataldo

{"title":"Neutrophil-Derived Interleukin 16 in Premetastatic Lungs Promotes Breast Tumor Cell Seeding.","authors":"Kim Donati, Christelle Sépult, Natacha Rocks, Silvia Blacher, Catherine Gérard, Agnès Noel, Didier Cataldo","doi":"10.1177/1179064417738513","DOIUrl":"10.1177/1179064417738513","url":null,"abstract":"The premetastatic niche in distant organs prior to metastatic cell arrival emerged as an important step in the metastatic cascade. However, molecular mechanisms underlying this process are still poorly understood. In particular, whether neutrophil recruitment at a premetastatic stage promotes or inhibits metastatic cell seeding has to be clarified. We aimed at unraveling how neutrophil infiltration in lung parenchyma induced by the distant primary tumor influences the establishment of lung metastasis. Elevated neutrophil counts and IL-16 levels were found in premetastatic lungs in a syngenic mouse model using 4T1 tumor cells. 4T1 cell-derived soluble factors stimulated IL-16 secretion by neutrophils. The functional contribution of IL-16 is supported by metastasis burden reduction in lungs observed on instillation of an IL-16 neutralizing antibody. Moreover, IL-16 promotes in vitro 4T1 cell adhesiveness, invasiveness, and migration. In conclusion, at a premetastatic stage, neutrophil-derived IL-16 favors tumor cell engraftment in lung parenchyma.","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"10 ","pages":"1179064417738513"},"PeriodicalIF":0.0,"publicationDate":"2017-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/55/9c/10.1177_1179064417738513.PMC5661667.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35241655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Upregulated Heat Shock Proteins After Hyperthermic Chemotherapy Point to Induced Cell Survival Mechanisms in Affected Tumor Cells From Peritoneal Carcinomatosis. 高温化疗后热休克蛋白的上调指向腹膜癌受影响肿瘤细胞诱导的细胞存活机制。

Cancer growth and metastasis Pub Date : 2017-09-18 eCollection Date: 2017-01-01 DOI: 10.1177/1179064417730559

Tanja Grimmig, Eva-Maria Moll, Kerstin Kloos, Rebecca Thumm, Romana Moench, Simone Callies, Jennifer Kreckel, Malte Vetterlein, Joerg Pelz, Buelent Polat, Sudipta Tripathi, Roberta Rehder, Carmen M Ribas, Anil Chandraker, Christoph-T Germer, Ana Maria Waaga-Gasser, Martin Gasser

{"title":"Upregulated Heat Shock Proteins After Hyperthermic Chemotherapy Point to Induced Cell Survival Mechanisms in Affected Tumor Cells From Peritoneal Carcinomatosis.","authors":"Tanja Grimmig, Eva-Maria Moll, Kerstin Kloos, Rebecca Thumm, Romana Moench, Simone Callies, Jennifer Kreckel, Malte Vetterlein, Joerg Pelz, Buelent Polat, Sudipta Tripathi, Roberta Rehder, Carmen M Ribas, Anil Chandraker, Christoph-T Germer, Ana Maria Waaga-Gasser, Martin Gasser","doi":"10.1177/1179064417730559","DOIUrl":"https://doi.org/10.1177/1179064417730559","url":null,"abstract":"In patients with peritoneal carcinomatosis cytoreductive surgery combined with hyperthermic intraperitoneal chemotherapy (HIPEC) represents a promising treatment strategy. Here, we studied the role of hyperthermic chemotherapy on heat shock protein (HSP) expression and induction of tumor cell death and survival. HSP27, HSP70, and HSP90 combined with effects on tumor cell proliferation and chemosensitivity were analyzed in human colon cancer. Hyperthermic chemotherapy resulted in significant HSP27/HSP70 and HSP90 gene/protein overexpression in analyzed HT-29/SW480/SW620 colon cancer cells and peritoneal metastases from patients displaying amplified expression of proliferation markers, proliferating cell nuclear antigen and antiapoptotic protein Bcl-xL. Moreover, functionally increased chemoresistance against 5-fluorouracil/mitomycin C and oxaliplatin after hyperthermic chemotherapy points to induced survival mechanisms in cancer cells. In conclusion, the results indicate that intracellular HSP-associated antiapoptotic and proliferative effects after hyperthermic chemotherapy negatively influence beneficial effects of hyperthermic chemotherapy-induced cell death. Therefore, blocking HSPs could be a promising strategy to further improve the rate of tumor cell death and outcome of patients undergoing HIPEC therapy.","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"10 ","pages":"1179064417730559"},"PeriodicalIF":0.0,"publicationDate":"2017-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179064417730559","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35796304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 23

Suppression of Breast Cancer Metastasis Using Stapled Peptides Targeting the WASF Regulatory Complex. 靶向WASF调控复合物的钉接肽抑制乳腺癌转移。

Cancer growth and metastasis Pub Date : 2017-06-19 eCollection Date: 2017-01-01 DOI: 10.1177/1179064417713197

John K Cowell, Yong Teng, N George Bendzunas, Roxan Ara, Ali S Arbab, Eileen J Kennedy

{"title":"Suppression of Breast Cancer Metastasis Using Stapled Peptides Targeting the WASF Regulatory Complex.","authors":"John K Cowell, Yong Teng, N George Bendzunas, Roxan Ara, Ali S Arbab, Eileen J Kennedy","doi":"10.1177/1179064417713197","DOIUrl":"https://doi.org/10.1177/1179064417713197","url":null,"abstract":"The WASF3 gene facilitates the metastatic phenotype, and its inactivation leads to suppression of invasion and metastasis regardless of the genetic background of the cancer cell. This reliance on WASF3 to facilitate metastasis suggests that targeting its function could serve as an effective strategy to suppress metastasis. WASF3 stability and function are regulated by the WASF Regulatory Complex (WRC) of proteins, particularly CYFIP1 and NCKAP1. Knockdown of these proteins in vitro leads to disruption of the WRC and suppression of invasion. We have used mouse xenograft models of breast cancer metastasis to assess whether targeting the WRC complex suppresses metastasis in vivo. Stapled peptides targeting the WASF3-CYFIP1 interface (WAHM1) and the CYFIP1-NCKAP1 interface (WANT3) suppress the development of lung and liver metastases. Targeting these critical protein-protein interactions, therefore, could potentially be developed into a therapeutic strategy to control cancer cell invasion and metastasis.","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"10 ","pages":"1179064417713197"},"PeriodicalIF":0.0,"publicationDate":"2017-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179064417713197","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35146909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 14

Inflammation and Epithelial-Mesenchymal Transition in Pancreatic Ductal Adenocarcinoma: Fighting Against Multiple Opponents. 胰腺导管腺癌的炎症和上皮-间质转化:对抗多种对手。

Cancer growth and metastasis Pub Date : 2017-05-15 eCollection Date: 2017-01-01 DOI: 10.1177/1179064417709287

Farid G Khalafalla, Mohammad W Khan

引用次数: 29