Advanced Research in Epithelial–Mesenchymal Transition (EMT) in Cancers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 927

Special Issue Editor


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Guest Editor
1. Department of Anatomy-Histology-Embryology, School of Medicine, University of Patras, Rion, Greece
2. Department of Surgery, University Hospital of Patras, Rion, Greece
Interests: molecular biology of breast cancer; epithelial–mesenchymal transition (EMT); Hippo pathway; integrin-linked kinase (ILK)

Special Issue Information

Dear Colleagues,

A typical PubMed query using the search term “epithelial–mesenchymal transition” (“EMT”) retrieves over 48.000 articles, a number that is indicative of the great interest in this topic. EMT is a reversible transdifferentiation program whereby epithelial cells acquire the invasive, migratory mesenchymal phenotype. EMT normally occurs during embryonic development, as well as in wound healing as a physiological response to injury. This embryonic genetic program is hijacked by cancer cells for their own benefit, favoring the acquisition of metastatic capacity and resistance to therapy. Initially considered to be an on–off phenomenon, EMT is now viewed as a gradual transformation process that also produces epithelial–mesenchymal hybrids through partial EMT. Once the metastatic cells that have undergone EMT reach the site of distant metastasis, they are believed to undergo the reverse process of mesenchymal–epithelial transition (MET) in order to increase their proliferative capacity and facilitate metastatic outgrowth. Thus, cancer cells through EMT/MET processes acquire cellular plasticity and the ability to interconvert between intermediate epithelial–mesenchymal cell states in order to fulfill the various spatial and temporal requirements during the course of malignant progression and metastasis. Importantly, except from motility and invasion, EMT has been associated with chemoresistance, cancer stem cell properties, resistance to apoptosis, genomic instability, and metabolic reprogramming.

In this Special Issue, we welcome the submission of both original research and review articles focused on the latest progress and recent findings in all aspects of cancer-related EMT.

Dr. Ioanna Akrida
Guest Editor

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Keywords

  • epithelial–mesenchymal transition (EMT)
  • mesenchymal–epithelial transition (MET)
  • epithelial–mesenchymal plasticity (EMP)
  • tumor microenvironment
  • cell–extracellular matrix interactions
  • extracellular matrix remodeling
  • metastasis

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Published Papers (1 paper)

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Research

18 pages, 6299 KiB  
Article
LncRNA RP11-297P16.4 Promotes the Invasion and Metastasis of Non-Small-Cell Lung Carcinoma by Targeting the miR-145-5p/MMP-2/9 Axis
by Wei Wang, Yu Lu, Guang-Mei Qin, Lin-Feng Ni, Bai-Xue Xu, Chao-Feng Liu, Bao-Feng Yu, Hai-Long Wang and Min Pang
Biomedicines 2025, 13(3), 617; https://doi.org/10.3390/biomedicines13030617 - 3 Mar 2025
Viewed by 677
Abstract
Background/Objectives: Long noncoding RNAs (lncRNAs) participate in the occurrence and development of non-small-cell lung carcinoma (NSCLC). But for certain lncRNAs, their effects on NSCLC remain unclear. This work discovered that lncRNA RP11-297P16.4 is elevated in NSCLC. Methods: LncRNA RP11-297P16.4 expression within LUAD tissues [...] Read more.
Background/Objectives: Long noncoding RNAs (lncRNAs) participate in the occurrence and development of non-small-cell lung carcinoma (NSCLC). But for certain lncRNAs, their effects on NSCLC remain unclear. This work discovered that lncRNA RP11-297P16.4 is elevated in NSCLC. Methods: LncRNA RP11-297P16.4 expression within LUAD tissues and cells was measured through RT-qPCR and Western blot. To assess the role of the lncRNA RP11-297P16.4 in NSCLC, gain- or loss-of-function experiments were conducted using an NSCLC mouse tumor model. Results: Silencing of the lncRNA RP11-297P16.4 inhibited the NSCLC cell line invasion and migration potential, but re-expression of the lncRNA RP11-297P16.4 had the opposite effect. A luciferase reporter confirmed that the lncRNA RP11-297P16.4 functions as a competitive endogenous RNA (ceRNA) through the sponge of miR-145-5p. The expression of lncRNA RP11-297P16.4 was negatively correlated to the level of miR-145-5p in NSCLC cells, which sponged miR-145-5p and suppressed tumor cell migration and invasion by targeting matrix metalloproteinase 2 (MMP-2) and MMP-9. Conclusions: Our findings suggested that the lncRNA RP11-297P16.4/miR-145-5p/MMP-2/9 regulatory axis is the key pathway for mediating the migration and invasion of NSCLC. Full article
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