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Journals
Biomolecules
Special Issues
Cellular Signaling in Cancer
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Cellular Signaling in Cancer

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 2094

Special Issue Editors

Dr. Avisek Majumder

E-Mail Website
Guest Editor
Department of Medicine, University of California, San Francisco, CA 94158, USA
Interests: HER3; SynNotch CAR-T cell therapy; HER2-positive breast tumors
Special Issues, Collections and Topics in MDPI journals
Dr. Shabana Bano

E-Mail Website
Guest Editor Assistant
Department of Medicine, University of California, San Francisco, CA 94158, USA
Interests: hydrogen sulfide (H2S); short-chain fatty acids (SCFAs); ulcerative colitis (UC); inflammation; diet; microbiome; cancer; therapy; Western diet; epigenetics; IBS; colorectal cancer; gut health
Dr. Kasturi Nayak

E-Mail
Guest Editor Assistant
Quantitative Biosciences Institute, Department of Medicine, University of California, San Francisco, CA 94158, USA
Interests: hydrogen sulfide (H2S); short-chain fatty acids (SCFAs); inflammation

Special Issue Information

Dear Colleagues,

Cancer is the second leading cause of death after cardiovascular disease, and despite the enormous efforts in advancing anti-cancer agents, it is still challenging to treat cancer. This multifaceted disease is characterized by six hallmarks: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. This Special Issue focuses on key signaling pathways involved in tumorigenesis, progression, and drug resistance. Several signaling pathways have been identified as frequently altered in cancer that led to uncontrolled cell proliferation, survival, and invasion, driving the disease's progression. Identifying the critical cellular signaling in cancer vs. normal cells can lead to the development of targeted therapy aimed at specific signaling molecules. Targeted therapy, whether used alone or in combination with other conventional treatments such as chemotherapy, radiotherapy, or surgery, can lead to more effective cancer therapies while minimizing the harmful effects on healthy cells. Advancements in various cancer types have arisen, with targeted approaches significantly improving patient outcomes. Continued research into cell signaling mechanisms holds promise for identifying novel therapeutic targets and improving cancer treatment strategies. As we deepen our understanding of the complexity and interactions within signaling pathways, personalized medicine may become a more standard form of cancer care, allowing for tailored treatments based on the unique molecular profiles of individual tumors.

Dr. Avisek Majumder
Guest Editor

Dr. Shabana Bano
Dr. Kasturi Nayak
Guest Editor Assistants

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. Biomolecules 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 2700 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

  • signaling pathways
  • cancer
  • anti-cancer

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Published Papers (2 papers)

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Review

24 pages, 4906 KiB  
Review
Modulating PAK1: Accessory Proteins as Promising Therapeutic Targets
by Amin Mirzaiebadizi, Rana Shafabakhsh and Mohammad Reza Ahmadian
Biomolecules 2025, 15(2), 242; https://doi.org/10.3390/biom15020242 - 7 Feb 2025
Viewed by 675
Abstract
The p21-activated kinase (PAK1), a serine/threonine protein kinase, is critical in regulating various cellular processes, including muscle contraction, neutrophil chemotaxis, neuronal polarization, and endothelial barrier function. Aberrant PAK1 activity has been implicated in the progression of several human diseases, including cancer, heart disease, [...] Read more.
The p21-activated kinase (PAK1), a serine/threonine protein kinase, is critical in regulating various cellular processes, including muscle contraction, neutrophil chemotaxis, neuronal polarization, and endothelial barrier function. Aberrant PAK1 activity has been implicated in the progression of several human diseases, including cancer, heart disease, and neurological disorders. Increased PAK1 expression is often associated with poor clinical prognosis, invasive tumor characteristics, and therapeutic resistance. Despite its importance, the cellular mechanisms that modulate PAK1 function remain poorly understood. Accessory proteins, essential for the precise assembly and temporal regulation of signaling pathways, offer unique advantages as therapeutic targets. Unlike core signaling components, these modulators can attenuate aberrant signaling without completely abolishing it, potentially restoring signaling to physiological levels. This review highlights PAK1 accessory proteins as promising and novel therapeutic targets, opening new horizons for disease treatment. Full article
(This article belongs to the Special Issue Cellular Signaling in Cancer)
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23 pages, 2343 KiB  
Review
Autophagy and Cancer: Insights into Molecular Mechanisms and Therapeutic Approaches for Chronic Myeloid Leukemia
by Mohd Adnan Kausar, Sadaf Anwar, Yusuf Saleem Khan, Ayman A. Saleh, Mai Ali Abdelfattah Ahmed, Simran Kaur, Naveed Iqbal, Waseem Ahmad Siddiqui and Mohammad Zeeshan Najm
Biomolecules 2025, 15(2), 215; https://doi.org/10.3390/biom15020215 - 2 Feb 2025
Viewed by 1092
Abstract
Autophagy is a critical cellular process that maintains homeostasis by recycling damaged or aberrant components. This process is orchestrated by a network of proteins that form autophagosomes, which engulf and degrade intracellular material. In cancer, autophagy plays a dual role: it suppresses tumor [...] Read more.
Autophagy is a critical cellular process that maintains homeostasis by recycling damaged or aberrant components. This process is orchestrated by a network of proteins that form autophagosomes, which engulf and degrade intracellular material. In cancer, autophagy plays a dual role: it suppresses tumor initiation in the early stages but supports tumor growth and survival in advanced stages. Chronic myeloid leukemia (CML), a hematological malignancy, is characterized by the Philadelphia chromosome, a chromosomal abnormality resulting from a translocation between chromosomes 9 and 22. Autophagy has emerged as a key factor in CML pathogenesis, promoting cancer cell survival and contributing to resistance against tyrosine kinase inhibitors (TKIs), the primary treatment for CML. Targeting autophagic pathways is being actively explored as a therapeutic approach to overcome drug resistance and enhance cancer cell death. Recent research highlights the intricate interplay between autophagy and CML progression, underscoring its role in disease biology and treatment outcomes. This review aims to provide a comprehensive analysis of the molecular and cellular mechanisms underlying CML, with a focus on the therapeutic potential of targeting autophagy. Full article
(This article belongs to the Special Issue Cellular Signaling in Cancer)
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