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Biological Hallmarks and Therapeutic Strategies in Cancer
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Biological Hallmarks and Therapeutic Strategies in Cancer

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: 20 November 2025 | Viewed by 1840

Special Issue Editor

Dr. Ramesh Kumar

E-Mail Website
Guest Editor
Institute of Molecular and Cell Biology, A*STAR (Agency for Science, Technology, and Research), Singapore 138673, Singapore
Interests: cell signaling; carcinogenesis; drug resistance; synthetic lethality; therapeutic targets; small molecule drug discovery

Special Issue Information

Dear Colleagues,

The hallmarks of cancer represent a set of functional capabilities acquired by normal cells towards the initiation of abnormal proliferative capabilities, induction of carcinogenesis, and the rise in malignant tumors. Originally, Hanahan and Weinberg proposed six acquired capabilities in 2000 and conducted research that resulted in two emerging hallmarks increasing to eight in 2011. These conceptualizations have enabled scientists to understand the distinctive stages of tumorigenesis and the characteristics needed to navigate through deep therapeutic exploration.

Cancer is a complex disease that is tightly regulated by cross-talk between various cell signaling. Cancer cells often switch to intrinsic and acquired resistance to escape from chemotherapeutic agents. The development of drug resistance is one of the key challenges to improving progression-free survival and overall survival among cancer patients. In this issue, we propose to present new information on a broad range of therapeutic targets and approaches to address this problem. In addition to target-specific inhibitors and degraders, we aim to present new information on the convergence of key oncogenic signaling, synthetic lethality, and combination therapy approaches to spread among the scientific community. Collectively, we invite manuscripts from researchers working in academic and industry research settings. I am looking forward to working with you.

Dr. Ramesh Kumar
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. 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

  • hallmarks of cancer
  • cancer progression
  • chemotherapy
  • tumorigenesis
  • oncogenic signaling

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Published Papers (2 papers)

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Research

20 pages, 1226 KiB  
Article
Transcriptomic Landscape of Paclitaxel-Induced Multidrug Resistance in 3D Cultures of Colon Cancer Cell Line DLD1
by Sandra Dragicevic, Jelena Dinic, Milena Ugrin, Marija Vidovic, Tamara Babic and Aleksandra Nikolic
Int. J. Mol. Sci. 2025, 26(14), 6580; https://doi.org/10.3390/ijms26146580 - 9 Jul 2025
Viewed by 335
Abstract
Multidrug resistance (MDR) significantly contributes to colon cancer recurrence, making it essential to understand its molecular basis for improved therapies. This study aimed to identify genes and pathways involved in resistance to standard chemotherapeutics by comparing transcriptome profiles of sensitive and paclitaxel-induced MDR [...] Read more.
Multidrug resistance (MDR) significantly contributes to colon cancer recurrence, making it essential to understand its molecular basis for improved therapies. This study aimed to identify genes and pathways involved in resistance to standard chemotherapeutics by comparing transcriptome profiles of sensitive and paclitaxel-induced MDR colonospheres. Cell viability and growth were assessed following treatment with 5-fluorouracil, oxaliplatin, irinotecan, bevacizumab, and cetuximab. Drug concentrations in culture media posttreatment were measured using high-performance liquid chromatography (HPLC). RNA sequencing (RNA-seq) of untreated sensitive and resistant colonospheres identified differentially expressed genes linked to baseline resistance. Our results confirmed cross-resistance in the resistant model, showing highest oxaliplatin tolerance may involve mechanisms beyond efflux. Transcriptome analysis highlighted upregulation of PIGR and activation of the ribosomal signaling pathway as potential resistance mediators. Notably, AKR1B10, a gene linked to chemotherapeutic detoxification, was overexpressed, whereas genes related to adhesion and membrane transport were downregulated. The overexpression of ribosomal protein genes suggests ribosome biogenesis plays a key role in acquired resistance. These findings suggest that targeting ribosome biogenesis and specific deregulated genes such as PIGR and AKR1B10 may offer promising strategies to overcome MDR in colon cancer. Full article
(This article belongs to the Special Issue Biological Hallmarks and Therapeutic Strategies in Cancer)
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25 pages, 2579 KiB  
Article
Exploring Carboxamide Derivatives as Promising Anticancer Agents: Design, In Vitro Evaluation, and Mechanistic Insights
by Manal M. Al-Najdawi, Maysaa M. Saleh, Dima A. Sabbah, Rima Hajjo, Hiba Zalloum, Suha M. Abudoleh, Duaa A. Abuarqoub, Yusuf M. Al-Hiari, Mohammad Yasin Mohammad, Husam ALSalamat, Hebah Mansour, Nawzat D. Aljbour and Aktham H. Mestareehi
Int. J. Mol. Sci. 2025, 26(12), 5903; https://doi.org/10.3390/ijms26125903 - 19 Jun 2025
Viewed by 733
Abstract
Carboxamide derivatives are a promising class of compounds in anticancer drug discovery, owing to their ability to interact with multiple oncogenic targets and their favorable pharmacological profiles. In this study, we report the design, synthesis, and biological evaluation of a series of N [...] Read more.
Carboxamide derivatives are a promising class of compounds in anticancer drug discovery, owing to their ability to interact with multiple oncogenic targets and their favorable pharmacological profiles. In this study, we report the design, synthesis, and biological evaluation of a series of N-substituted 1H-indole-2-carboxamides as potential anticancer agents. The synthesized compounds were assessed for antiproliferative activity using the MTT assay against MCF-7 (breast cancer), K-562 (leukemia), and HCT-116 (colon cancer) cell lines, with normal human dermal fibroblasts included as a non-cancerous control. Several compounds demonstrated notable cytotoxicity and selectivity. Compounds 12, 14, and 4 exhibited potent activity against K-562 cells, with IC50 values of 0.33 µM, 0.61 µM, and 0.61 µM, respectively. Compound 10 showed the most significant activity against HCT-116 cells (IC50 = 1.01 µM) with a high selectivity index (SI = 99.4). Moderate cytotoxicity was observed against MCF-7 cells. To elucidate the mechanism of action, molecular docking and induced-fit docking studies were conducted against key cancer-related targets, including topoisomerase–DNA (PDB ID: 5ZRF), PI3Kα (4L23), and EGFR (3W32), revealing favorable binding interactions. Additionally, principal component analysis of molecular descriptors indicated that the compounds possess promising drug-like and lead-like properties, particularly compound 10. Overall, this study highlights N-substituted indole-2-carboxamides as promising scaffolds for further optimization. The integration of synthetic chemistry, biological assays, and computational modeling provides a robust foundation for the continued development of these compounds as potential anticancer agents. Full article
(This article belongs to the Special Issue Biological Hallmarks and Therapeutic Strategies in Cancer)
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