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Peer-reviewedCC BY-NC-NDJournal of dental sciences

A bibliometric evolution of molecular mechanisms and emerging research trends of therapeutic resistance in oral cancer.

  • Chu-Yen Chien1
  • Ying-Chen Chen2
  • Jia-Rong Wu3
  • Hsu-Hua Chu4
  • Yi-Jen Hung5
  • Yi-Shing Shieh3,6
6 affiliations
  1. 1Graduate Institute of Medical Sciences, National Defense Medical University, Taipei, Taiwan.
  2. 2Molecular and Cell Biology, Taiwan International Graduate Program, Academia Sinica and Graduate Institute of Life Science, National Defense Medical University, Taipei, Taiwan.
  3. 3Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan.
  4. 4Department of Risk Management and Insurance, National Chengchi University, Taipei, Taiwan.
  5. 5Division of Endocrinology and Metabolism, Tri-Service General Hospital, National Defense Medical University, Taipei, Taiwan.
  6. 6Department of Dentistry, Tri-Service General Hospital, National Defense Medical University, Taipei, Taiwan.
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Abstract

Background/purpose

Drug resistance has served as a primary determinant of treatment failure and disease recurrence in oral cancer. The present study aimed to evaluate the global research landscape of drug resistance mechanisms in oral cancer by integrating bibliometric mapping with bioinformatic validation.Materials and methods

A comprehensive dataset of 1660 publications was retrieved from the Scopus database. Bibliometric analyses were performed using Biblioshiny and VOSviewer to evaluate publication trends, collaborative networks, and thematic evolution. To bridge research trends with biological mechanisms, 1469 genes associated with oral cancer and drug resistance were extracted from the GeneCards database and subjected to functional enrichment and canonical pathway analysis via Ingenuity Pathway Analysis (IPA).Results

Bibliometric mapping revealed a significant shift from basic cell-intrinsic molecules toward complex themes, including tumor microenvironment (TME), intercellular communications, cancer stem cells (CSCs), and non-coding RNA networks. Frequency distribution analysis identified microRNA as the most prevalent mediator, highlighting the principal role of post-transcriptional regulation. Furthermore, CSCs and epithelial-mesenchymal transition (EMT) emerged as major thematic hubs within the co-occurrence network. GeneCards analysis identified ABCB1, ABCG2, EGFR, and STAT3 as central hubs with high relevance scores. IPA further validated these findings, demonstrating dense crosstalk between TME and EMT-related pathways as the mechanistic foundation of therapeutic escape.Conclusion

The study demonstrated oral cancer resistance is governed by signaling redundancy and microenvironmental protection rather than an individual biological aberration. Consequently, future researches are needed to investigate intercellular crosstalk and cellular heterogeneity in oral cancer to circumvent the multifaceted barriers driving current therapeutic failure.

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Cite

BibTeXRIS
BibTeX
@article{chien2026bibliometric,
  title = {{A bibliometric evolution of molecular mechanisms and emerging research trends of therapeutic resistance in oral cancer.}},
  author = {Chu-Yen Chien and Ying-Chen Chen and Jia-Rong Wu and Hsu-Hua Chu and Yi-Jen Hung and Yi-Shing Shieh},
  journal = {Journal of dental sciences},
  year = {2026},
  month = oct,
  doi = {10.1016/j.jds.2025.07.3587},
  url = {https://europepmc.org/article/MED/42924173},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - A bibliometric evolution of molecular mechanisms and emerging research trends of therapeutic resistance in oral cancer.
AU  - Chu-Yen Chien
AU  - Ying-Chen Chen
AU  - Jia-Rong Wu
AU  - Hsu-Hua Chu
AU  - Yi-Jen Hung
AU  - Yi-Shing Shieh
PY  - 2026
DA  - 2026/10/01
JO  - Journal of dental sciences
DO  - 10.1016/j.jds.2025.07.3587
UR  - https://europepmc.org/article/MED/42924173
AB  - Background/purpose  Drug resistance has served as a primary determinant of treatment failure and disease recurrence in oral cancer. The present study aimed to evaluate the global research landscape of drug resistance mechanisms in oral cancer by integrating bibliometric mapping with bioinformatic validation.Materials and methods  A comprehensive dataset of 1660 publications was retrieved from the Scopus database. Bibliometric analyses were performed using Biblioshiny and VOSviewer to evaluate publication trends, collaborative networks, and thematic evolution. To bridge research trends with biological mechanisms, 1469 genes associated with oral cancer and drug resistance were extracted from the GeneCards database and subjected to functional enrichment and canonical pathway analysis via Ingenuity Pathway Analysis (IPA).Results  Bibliometric mapping revealed a significant shift from basic cell-intrinsic molecules toward complex themes, including tumor microenvironment (TME), intercellular communications, cancer stem cells (CSCs), and non-coding RNA networks. Frequency distribution analysis identified microRNA as the most prevalent mediator, highlighting the principal role of post-transcriptional regulation. Furthermore, CSCs and epithelial-mesenchymal transition (EMT) emerged as major thematic hubs within the co-occurrence network. GeneCards analysis identified ABCB1, ABCG2, EGFR, and STAT3 as central hubs with high relevance scores. IPA further validated these findings, demonstrating dense crosstalk between TME and EMT-related pathways as the mechanistic foundation of therapeutic escape.Conclusion  The study demonstrated oral cancer resistance is governed by signaling redundancy and microenvironmental protection rather than an individual biological aberration. Consequently, future researches are needed to investigate intercellular crosstalk and cellular heterogeneity in oral cancer to circumvent the multifaceted barriers driving current therapeutic failure.
SN  - 1991-7902
SN  - 2213-8862
ER  -