ijms-logo

Journal Browser

Journal Browser

Molecular Mechanisms and Pathways of Epithelial-Mesenchymal Transition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 672

Special Issue Editor


E-Mail Website
Guest Editor
Department of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy
Interests: cancer biology; tumor microenvironment; inositols; weightlessness; fibrosis; EMT; breast cancer; systems biology

Special Issue Information

Dear Colleagues,

Epithelial-to-mesenchymal transition (EMT) is a fundamental biological process by which epithelial cells undergo several morphological modifications enabling them to acquire mesenchymal properties. This process is a complex and multifaceted process involved in both normal development and disease, including fibrosis, cancer progression and metastasis, and therapy resistance.

This Special Issue aims to provide a comprehensive overview of the molecular mechanisms and regulatory networks governing EMT. We welcome contributions focusing on signaling pathways, transcriptional and epigenetic regulation, cellular plasticity, and EMT-related biomarkers. Particularly, it is time to design properly tailored pharmacological countermeasures in order to antagonize such a process, namely by manipulating the cancer microenvironment. Therefore, studies offering novel mechanistic insights or therapeutic implications in pathological EMT contexts are particularly encouraged.

Dr. Noemi Monti
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • metastasis
  • fibrosis
  • tumor microenvironment
  • molecular pathways
  • EMT reversion

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:
28 pages, 12625 KB  
Article
Tedizolid Targets AQP9-JAK/STAT Axis to Suppress Metastatic Progression in Clear Cell Renal Cell Carcinoma: Mechanism and Therapeutic Implications
by Kexin Qu, Tianya Zhang, Rui Wang, Yingwei Bi, Jiacheng Jin, Yuxin Liu, Bolin Yi, Liang Zhu and Jianbo Wang
Int. J. Mol. Sci. 2026, 27(10), 4234; https://doi.org/10.3390/ijms27104234 - 9 May 2026
Viewed by 280
Abstract
Metastasis is a primary driver of poor outcomes in clear cell renal cell carcinoma (ccRCC), yet the role of Aquaporin-9 (AQP9) in this process remains unclear. This study aimed to investigate the function, clinical significance, and therapeutic potential of AQP9 in ccRCC. AQP9 [...] Read more.
Metastasis is a primary driver of poor outcomes in clear cell renal cell carcinoma (ccRCC), yet the role of Aquaporin-9 (AQP9) in this process remains unclear. This study aimed to investigate the function, clinical significance, and therapeutic potential of AQP9 in ccRCC. AQP9 expression was analyzed using TCGA data and validated in human tissues and cell lines via Western blot. Functional assays assessed malignant behaviors, while bioinformatics and rescue experiments explored the involvement of the JAK/STAT pathway and epithelial–mesenchymal transition (EMT). Virtual screening, molecular docking, and cellular thermal shift assays (CETSAs) were employed to identify Tedizolid as a potential AQP9 inhibitor, followed by functional validation in vitro and in a xenograft model. AQP9 was significantly upregulated in ccRCC and associated with poor prognosis. The knockdown of AQP9 suppressed proliferation, migration, invasion, and EMT, whereas its overexpression promoted these effects by activating the JAK/STAT pathway. Tedizolid bound directly to AQP9, inhibited cell viability, reversed AQP9-induced malignant phenotypes, and suppressed JAK/STAT signaling both in vitro and in vivo. In conclusion, AQP9 promotes ccRCC metastasis through the JAK/STAT-EMT axis and represents a potential prognostic biomarker and therapeutic target. Tedizolid, identified as a novel AQP9 inhibitor, offers a promising repurposed strategy for ccRCC treatment. Full article
Show Figures

Figure 1

Back to TopTop