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Innovative Biological Molecules for Cancer Therapy
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Innovative Biological Molecules for Cancer Therapy

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: closed (25 March 2025) | Viewed by 1332

Special Issue Editor

Dr. Ming-Ju Hsieh

E-Mail Website
Guest Editor
Oral Cancer Research Center, Changhua Christian Hospital, Changhua 500, Taiwan
Interests: apoptosis; autophagy; metastasis; anti-cancer; nature compound; cell biochemistry
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, titled “Innovative Biological Molecules for Cancer Therapy”, focuses on the latest breakthroughs in the development of new biological molecules that offer promising advances in cancer treatment.   This issue aims to compile cutting-edge research on molecules that can effectively inhibit or slow tumor growth and prevent cancer spread with fewer toxic side effects than traditional therapies.   The focus is on exploring diverse molecular strategies that improve the precision and efficacy of cancer treatment, leading to better patient outcomes.   This Special Issue will highlight innovative approaches to creating and using biological molecules, such as antibodies, peptides, and nucleic acid-based therapies, that target cancer cells more selectively while minimizing damage to healthy tissues.   By improving the specificity and reducing the toxicity of cancer therapies, these novel molecules have the potential to significantly advance current therapeutic strategies.

Therefore, contributions that investigate the design, development, and clinical application of these molecules and their integration into existing treatment protocols are particularly encouraged.   This Special Issue will serve as a comprehensive resource for researchers, clinicians, and pharmaceutical professionals, providing information on the next generation of cancer therapies and their potential to transform the landscape of oncology.

Dr. Ming-Ju Hsieh
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

  • cancer treatment
  • immunotherapy
  • biological therapy
  • natural products
  • active molecule
  • biological peptide
  • antibody
  • nucleic acid
  • pharmacology

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Published Papers (2 papers)

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Research

17 pages, 3166 KiB  
Article
Synergistic Anti-Cancer Activity of Melittin and Erlotinib in Non-Small Cell Lung Cancer
by Hairulislam M. Ibrahim, Jihad Alessa, Hala Badr Khalil, Gamal A. Bekhet and Ashraf Khalifa
Int. J. Mol. Sci. 2025, 26(7), 2903; https://doi.org/10.3390/ijms26072903 - 22 Mar 2025
Viewed by 396
Abstract
Lung cancer remains a leading cause of cancer-related mortality worldwide. Despite advancements in current therapies, the development of drug resistance and the need for improved treatment outcomes necessitate the exploration of novel therapeutic approaches. This study aimed to investigate the synergistic anti-cancer effects [...] Read more.
Lung cancer remains a leading cause of cancer-related mortality worldwide. Despite advancements in current therapies, the development of drug resistance and the need for improved treatment outcomes necessitate the exploration of novel therapeutic approaches. This study aimed to investigate the synergistic anti-cancer effects of Melittin, a bee venom peptide, in combination with Erlotinib, an EGFR inhibitor, in non-small cell lung cancer (NSCLC). The study evaluated the combined effects of Melittin and Erlotinib on A549 NSCLC cells. Cell viability, proliferation, migration, and apoptosis were assessed using standard in vitro assays. Mechanistic studies investigated the impact of the combination treatment on key signaling pathways, including those involving JAK2 and JAK3. Molecular docking simulations were performed to predict the binding interactions between Melittin and these kinases. The combination of Melittin and Erlotinib significantly inhibited A549 cell proliferation and migration, with a marked reduction in cell viability and enhanced apoptosis compared to either agent alone. Mechanistically, Melittin demonstrated interactions with JAK2 and JAK3, key proteins involved in apoptotic signaling. Molecular docking simulations further supported these findings, predicting strong binding affinities between Melittin and both kinases. These findings demonstrate a synergistic anti-cancer effect of Melittin and Erlotinib in A549 NSCLC cells. The observed interactions with JAK2 and JAK3 suggest a potential mechanism for Melittin’s activity. These results highlight the potential of Melittin as a promising adjuvant to Erlotinib for the treatment of NSCLC. Full article
(This article belongs to the Special Issue Innovative Biological Molecules for Cancer Therapy)
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20 pages, 4515 KiB  
Article
Dinaciclib Interrupts Cell Cycle and Induces Apoptosis in Oral Squamous Cell Carcinoma: Mechanistic Insights and Therapeutic Potential
by Muhammet Oner, Yu-Chiao Cheng, Shiuan-Woei Soong, Pang-Ting Cheng, Yan-Hsiung Wang, Shun-Fa Yang, Stella Chin-Shaw Tsai and Ho Lin
Int. J. Mol. Sci. 2025, 26(5), 2197; https://doi.org/10.3390/ijms26052197 - 28 Feb 2025
Viewed by 531
Abstract
Dinaciclib, a potent cyclin-dependent kinase (CDK) inhibitor, has demonstrated considerable antitumor effects in various malignancies. However, its impact on oral squamous cell carcinoma (OSCC), a predominant and highly aggressive form of head and neck squamous cell carcinoma (HNSC) with limited treatment options, remains [...] Read more.
Dinaciclib, a potent cyclin-dependent kinase (CDK) inhibitor, has demonstrated considerable antitumor effects in various malignancies. However, its impact on oral squamous cell carcinoma (OSCC), a predominant and highly aggressive form of head and neck squamous cell carcinoma (HNSC) with limited treatment options, remains underexplored. We conducted gene set enrichment analyses in HNSC patients that reinforced the relevance of these cell cycle-related genes to OSCC pathogenesis. Given the known dysregulation of cell cycle-related genes in HNSC patients, we hypothesized that Dinaciclib may inhibit OSCC growth by targeting overexpressed cyclins and CDKs, thereby disrupting cell cycle progression and inducing apoptosis. This study investigated Dinaciclib’s effects on cell proliferation, cell cycle progression, and apoptosis in the OSCC cell lines Ca9-22, OECM-1, and HSC-3. Our results demonstrated that Dinaciclib significantly reduces OSCC cell proliferation in a dose-dependent manner. Flow cytometry and Western blot analyses showed that Dinaciclib induces cell cycle arrest at the G1/S and G2/M transitions by downregulating Cyclins A, B, D, and E, along with CDKs 1 and 2—key regulators of these checkpoints. Furthermore, Dinaciclib treatment upregulated apoptotic markers, such as cleaved-caspase-3 and cleaved-PARP, confirming its pro-apoptotic effects. In conclusion, these findings highlight Dinaciclib’s therapeutic promise in OSCC by simultaneously disrupting cell cycle progression and inducing apoptosis. These results support further exploration of Dinaciclib as a viable monotherapy or combination treatment in OSCC and other HNSC subtypes to improve patient outcomes. Full article
(This article belongs to the Special Issue Innovative Biological Molecules for Cancer Therapy)
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