EMT and inflammation: inseparable actors of cancer progression
TLDR
The interconnections between EMT programs and cellular and molecular actors of inflammation are described, and data linking the EMT/inflammation axis to metastasis is recapitulate.About:
This article is published in Molecular Oncology.The article was published on 2017-07-01 and is currently open access. It has received 368 citations till now. The article focuses on the topics: Epithelial–mesenchymal transition & Cancer cell.read more
Citations
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Inflammation and Cancer: Triggers, Mechanisms, and Consequences.
TL;DR: How tumor-promoting inflammation closely resembles inflammatory processes typically found during development, immunity, maintenance of tissue homeostasis, or tissue repair is discussed and the distinctions between tissue-protective and pro-tumorigenic inflammation are illuminated.
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Crosstalk between cancer cells and tumor associated macrophages is required for mesenchymal circulating tumor cell-mediated colorectal cancer metastasis
Chen Wei,Chaogang Yang,Shuyi Wang,Dongdong Shi,Chunxiao Zhang,Xiaobin Lin,Qing Liu,Rongzhang Dou,Bin Xiong +8 more
TL;DR: It is indicated that TAMs induce EMT program to enhance CRC migration, invasion, and CTC-mediated metastasis by regulating the JAK2/STAT3/miR-506-3p/FoxQ1 axis, which in turn leads to the production of CCL2 that promote macrophage recruitment, revealing a new cross-talk between immune cells and tumor cells in CRC microenvironment.
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The multifaceted role of chromosomal instability in cancer and its microenvironment
TL;DR: These multipronged effects distinguish CIN as a central driver of tumor evolution and as a genomic source for the crosstalk between the tumor and its microenvironment, in the course of immune editing and evasion.
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Contribution of Angiogenesis to Inflammation and Cancer.
Dolores Aguilar-Cazares,Rodolfo Chavez-Dominguez,Ángeles Carlos-Reyes,César López-Camarillo,Olga N Hernadez de la Cruz,Jose Sullivan Lopez-Gonzalez +5 more
TL;DR: The role of hypoxia as a mechanism that drives the acquisition of tumor hallmarks that make certain cancers more aggressive is discussed and some combinations of therapies that inhibit the angiogenesis process and that may be a successful strategy for cancer patients are indicated.
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miR-195-5p/NOTCH2-mediated EMT modulates IL-4 secretion in colorectal cancer to affect M2-like TAM polarization
Xiaobin Lin,Shuyi Wang,Min Sun,Min Sun,Chunxiao Zhang,Chen Wei,Chaogang Yang,Rongzhang Dou,Qing Liu,Bin Xiong +9 more
TL;DR: miR-195-5p may play a vital role in regulating NOTCH2-mediated tumor cell EMT, thereby affecting IL-4-related M2-like TAM polarization in CRC.
References
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SNAI1-mediated epithelial-mesenchymal transition confers chemoresistance and cellular plasticity by regulating genes involved in cell death and stem cell maintenance.
TL;DR: It is found that EMT induction in MCF10A cells by stably expressing SNAI1 contributed to drug resistance and acquisition of stem/progenitor-like character as shown by increased cell population for surface marker CD44+/CD24− and mammosphere forming capacity.
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Induction of reactive oxygen species generation inhibits epithelial-mesenchymal transition and promotes growth arrest in prostate cancer cells.
TL;DR: It is suggested that increasing the threshold of intracellular ROS could prevent or treat CaP growth and metastasis.
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Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity
Sabina Sangaletti,Claudio Tripodo,Alessandra Santangelo,Nadia Castioni,Paola Portararo,Alessandro Gulino,Laura Botti,Mariella Parenza,Barbara Cappetti,Rosaria Orlandi,Elda Tagliabue,Claudia Chiodoni,Mario P. Colombo +12 more
TL;DR: It is concluded that that SPARC is regulating the interplay between MDSCs and the ECM to drive the induction of EMT in tumor cells, rendering SPARC-overexpressing tumor cells sensitive to Doxil.
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Downregulation of HuR as a new mechanism of doxorubicin resistance in breast cancer cells
Elisa Latorre,Toma Tebaldi,Gabriella Viero,Antonino Maria Sparta,Alessandro Quattrone,Alessandro Provenzani +5 more
TL;DR: It is shown that HuR is necessary to elicit the apoptotic cell response to doxorubicin and that restoration of HuR expression in resistant cells resensitizes them to the action of this drug, thereby identifying HuR as a key protein in doxorbicin pharmacology.
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CD133+ ovarian cancer stem-like cells promote non-stem cancer cell metastasis via CCL5 induced epithelial-mesenchymal transition.
Haixia Long,Tong Xiang,Wei Qi,Jiani Huang,Junying Chen,Luhang He,Zhiqing Liang,Bo Guo,Yongsheng Li,Rongkai Xie,Bo Zhu +10 more
TL;DR: The results redefine the metastatic potential of non-stem cancer cells and provide evidence that targeting the CCL5:CCR1/3/5-NF-κB pathway could be an effective strategy to prevent ovarian cancer metastasis.