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Pharmaceuticals
Special Issues
Epithelial Plasticity and Therapy Resistance in Cancer
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Epithelial Plasticity and Therapy Resistance in Cancer

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 25 November 2025 | Viewed by 774

Special Issue Editor

Dr. Naisana Seyedasli

E-Mail Website
Guest Editor
School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Westmead Hospital, Westmead, NSW 2145, Australia
Interests: cancer biology; stem cells; developmental biology; regenerative biology

Special Issue Information

Dear Colleagues,

A major proportion of cancers originate from the epithelial tissue. The carcinogenic process is often induced by a disturbance in the balance of epithelial homeostasis, accompanied by the dedifferentiation of the epithelial state and increased plasticity. The pathogenic plasticity of the epithelial tissue is known to be associated with cancer progression, metastasis, and resistance to therapy. This Special Issue will focus on the processes within, and mechanistic links among, epithelial plasticity, carcinogenesis, and resistance to therapy.

Dr. Naisana Seyedasli
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. Pharmaceuticals is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • cancer stem cells
  • epithelial–mesenchymal transition
  • epithelial reprogramming
  • resistance
  • drug targets
  • resistance mechanisms
  • biomarker discovery

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Published Papers (1 paper)

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Research

18 pages, 3771 KB  
Article
VDR Decrease Enhances the Efficacy of 1,25-Dihydroxyvitamin D3 Inhibiting Gefitinib Resistance by Regulating EGFR/FASN Loop in NSCLC Cells
by Junqing Yang, Mingyu Fang, Mengjun Hou, Yalei Duan, Jiali Wang, Kaiyong Hu, Shuo Liu, Xiaoying Liu, Xiaohan Peng, Xuansheng Ding and Zhirong Jia
Pharmaceuticals 2025, 18(8), 1238; https://doi.org/10.3390/ph18081238 - 21 Aug 2025
Viewed by 544
Abstract
Background: Gefitinib is a first-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) targeting EGFR-mutated non-small cell lung cancer (NSCLC) and is a current first-line treatment for NSCLC. However, acquired resistance leads to the failure of treatment and remains a challenge. Therefore, [...] Read more.
Background: Gefitinib is a first-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) targeting EGFR-mutated non-small cell lung cancer (NSCLC) and is a current first-line treatment for NSCLC. However, acquired resistance leads to the failure of treatment and remains a challenge. Therefore, identifying novel therapeutic approaches to combat EGFR-TKI resistance is crucial. Methods: The Cancer Genome Atlas (TCGA) database analysis and gefitinib-resistant cell lines were used to analyze VDR expression in NSCLC. Cell proliferation and apoptosis were assessed via MTT assay, colony formation assay, and flow cytometry. Immunofluorescence, qPCR, and Western blotting were used to measure mRNA and protein expression levels of VDR and other related molecules. Xenograft tumors in BALB/c nude mice were employed to investigate the effects of VDR and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on gefitinib-resistant tumors in vivo. Results: We found that VDR was significantly upregulated in EGFR-TKI-resistant NSCLC cells. Patients with high VDR expression exhibited poor prognosis. VDR knockdown significantly inhibited cell proliferation, tumor growth, and reduced gefitinib resistance, whereas VDR overexpression enhanced resistance. VDR knockdown downregulated EGFR and FASN expression. Silencing either EGFR or FASN confirmed the existence of a positive feedback regulatory loop involving VDR, EGFR, and FASN. Treatment with 1,25(OH)2D3 increased VDR levels but decreased EGFR and FASN expression. VDR knockdown significantly enhanced the inhibitory effect of 1,25(OH)2D3 on gefitinib resistance. The combination of VDR knockdown and 1,25(OH)2D3 treatment was more effective than either treatment alone in suppressing EGFR and FASN expression. Conclusions: VDR promotes NSCLC resistance to EGFR-TKIs by regulating EGFR and FASN expression through a positive feedback loop. Knocking down VDR effectively enhances the ability of 1,25(OH)2D3 to overcome gefitinib resistance, mediated by the synergistic downregulation of EGFR and FASN expression. Targeting VDR represents a potential strategy to enhance the efficacy of 1,25(OH)2D3 in overcoming EGFR-TKI resistance. Full article
(This article belongs to the Special Issue Epithelial Plasticity and Therapy Resistance in Cancer)
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