scispace - formally typeset
Open AccessJournal ArticleDOI

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
More filters
Journal ArticleDOI

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.
Journal ArticleDOI

Crosstalk between cancer cells and tumor associated macrophages is required for mesenchymal circulating tumor cell-mediated colorectal cancer metastasis

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.
Journal ArticleDOI

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.
Journal ArticleDOI

Contribution of Angiogenesis to Inflammation and Cancer.

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.
Journal ArticleDOI

miR-195-5p/NOTCH2-mediated EMT modulates IL-4 secretion in colorectal cancer to affect M2-like TAM polarization

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
More filters
Journal ArticleDOI

Hypoxia-Induced Epithelial-to-Mesenchymal Transition in Hepatocellular Carcinoma Induces an Immunosuppressive Tumor Microenvironment to Promote Metastasis

TL;DR: It is suggested that the HIF-1α/CCL20/IDO axis in hepatocellular carcinoma is important for accelerating tumor metastasis through both the induction of EMT and the establishment of an immunosuppressive tumor microenvironment, warranting further investigation into the therapeutic effects of blocking specific nodes of this signaling network.
Journal ArticleDOI

Targeting the androgen receptor with siRNA promotes prostate cancer metastasis through enhanced macrophage recruitment via CCL2/CCR2-induced STAT3 activation

TL;DR: A novel therapeutic approach may be provided to better battle PCa progression and metastasis at the castration resistant stage via the combination of targeting AR with siRNA and anti‐CCL2/CCR2‐STAT3 signalling.
Journal ArticleDOI

The immune checkpoint ligand PD-L1 is upregulated in EMT-activated human breast cancer cells by a mechanism involving ZEB-1 and miR-200

TL;DR: It is proposed that PD-L1 expression in E MT-activated breast cancer cells depends on the EMT-TF involved in EMT activation, and this results provide a novel preclinical rationale to explore EMT inhibitors as adjuvants to boost immunotherapeutic responses in subgroups of patients in whom malignant progression is driven by different EMTs.
Journal ArticleDOI

Mechanisms of TGFβ-Induced Epithelial–Mesenchymal Transition

TL;DR: The key principles of the circuits that control EMT under the influence of TGFβ are illustrated, which include the ability to perform two parallel molecular functions, and to mediate signaling crosstalk with other developmental signaling pathways.
Journal ArticleDOI

IL-6 Secreted from Cancer-Associated Fibroblasts Mediates Chemoresistance in NSCLC by Increasing Epithelial-Mesenchymal Transition Signaling.

TL;DR: IL‐6 may contribute to maintenance of a paracrine loop that functions as part of the communication between CAFs and NSCLC cells, resulting in chemoresistance.
Related Papers (5)