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Cancer-Driving Molecules: From Molecular Mechanisms to Novel Therapeutics

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

Deadline for manuscript submissions: 30 November 2025 | Viewed by 744

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Guest Editor
Department of Chemistry, University of the Pacific, Stockton, CA 95211, USA
Interests: structural biology; drug discovery; cancer biology; protein dynamics
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Special Issue Information

Dear Colleagues,

Insights into the tumor microenvironment have led to the development of targeted therapies that not only extend the lifespan of cancer patients but also improve their quality of life. In some cancers, targeted therapies have displaced standard-of-care treatment plans, whereas in others, cytotoxic and targeted therapies are used in combination to enhance efficacy and address tumor heterogeneity. The success of targeted therapies is supported by a comprehensive analysis of cancer-driving  molecules, which are found in the tumor microenvironment. The structural and/or functional modification of such molecules has been shown to manipulate the immune system, promoting cancer cell survival and metastasis. Therefore, an in-depth characterization of these molecules could facilitate the discovery of next-generation therapeutics, further enhancing personalized treatment plans and expanding options for patients with advanced metastatic cancers.

This Special Issue entitled “Cancer-Driving Molecules: From Molecular Mechanisms to Novel Therapeutics” is open to original articles, short communications, case reports, and reviews from all the areas of cancer research. We welcome studies that provide insights into any type of oncogenic protein or protein complex, including but not limited to protein–protein, protein–ligand, protein–DNA, and protein–RNA interactions. Submissions focused on drug discovery at the preclinical stage, as well as studies utilizing checkpoint inhibitors or other mechanistic probes, are also encouraged. Examples of molecules within the scope of this Special Issue include CD receptors (e.g., CD19, CD40, CD47, CD74, and CD137), cytokines (e.g., MIF, D-DT, IFN-γ, TNF-α, and various interleukins), chemokines (e.g., CXCLs and CCLs), and chemokine receptors (e.g., CXCRs and CCRs). We also welcome studies on RNA- or DNA-binding proteins (e.g., YTHDF2 and BRCA1), cell death-related proteins (e.g., BCL2 and caspases), oncogenic enzymes (e.g., IDO, KRAS, NQO1, and IDH1), and ubiquitin-related proteins (e.g., E3 ligases). Checkpoint proteins (e.g., PD-1/PD-L1), transcription factors (e.g., STAT3 and MYC), kinases (e.g., ROS1 and NTRK1), members of the epidermal growth factor receptor (EGFR) family (e.g., HER1–4), bromodomain-containing proteins (e.g., BRD4), and many others are also of interest.

Dr. Georgios Pantouris
Guest Editor

Manuscript Submission Information

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Keywords

  • cancer
  • mechanism of action
  • tumor microenvironment
  • immune system
  • DNA/RNA/protein
  • small-molecule probes
  • activation/inhibition
  • biological activity

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Research

28 pages, 3546 KB  
Article
SCAMP3-Driven Regulation of ERK1/2 and Autophagy Phosphoproteomics Signatures in Triple-Negative Breast Cancer
by Beatriz M. Morales-Cabán, Yadira M. Cantres-Rosario, Eduardo L. Tosado-Rodríguez, Abiel Roche-Lima, Loyda M. Meléndez, Nawal M. Boukli and Ivette J. Suarez-Arroyo
Int. J. Mol. Sci. 2025, 26(19), 9577; https://doi.org/10.3390/ijms26199577 - 1 Oct 2025
Viewed by 453
Abstract
Extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitors show therapeutic potential in triple-negative breast cancer (TNBC), but resistance through compensatory signaling limits their efficacy. We previously identified the secretory carrier membrane protein 3 (SCAMP3) as a regulator of TNBC progression and ERK1/2 activation. Here, we [...] Read more.
Extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitors show therapeutic potential in triple-negative breast cancer (TNBC), but resistance through compensatory signaling limits their efficacy. We previously identified the secretory carrier membrane protein 3 (SCAMP3) as a regulator of TNBC progression and ERK1/2 activation. Here, we investigated the role of SCAMP3 in ERK1/2 signaling and therapeutic response using TMT-based LC-MS/MS phosphoproteomics of wild-type (WT) and SCAMP3 knockout (SC3KO) SUM-149 cells under basal conditions, after epidermal growth factor (EGF) stimulation, and during ERK1/2 inhibition with MK-8353. A total of 4408 phosphosites were quantified, with 1093 significantly changed. SC3KO abolished residual ERK activity under MK-8353 and affected the compensatory activation of oncogenic pathways observed in WT cells. SC3KO reduced the phosphorylation of ERK feedback regulators RAF proto-oncogene serine/threonine-protein kinase Raf-1 (S43) and the dual-specificity mitogen-activated protein kinase kinase 2 (MEK2) (T394), affected other ERK targets, including nucleoporins, transcription factors, and metabolic enzymes triosephosphate isomerase (TPI1) (S21) and ATP-citrate lyase (ACLY) (S455). SCAMP3 loss also impaired the mammalian target of rapamycin complex I (mTORC1) signaling and disrupted autophagic flux, evidenced by elevated sequestosome-1 (SQSTM1/p62) and microtubule-associated protein light chain 3 (LC3B-II) with reduced levels of the autophagosome lysosome maturation marker, Rab7A. Beyond ERK substrates, SC3KO affected phosphorylation events mediated by other kinases. These findings position SCAMP3 as a central coordinator of ERK signaling and autophagy. Our results support SCAMP3 as a potential therapeutic target to enhance ERK1/2 inhibitor clinical efficacy and overcome adaptive resistance mechanisms in TNBC. Full article
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