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Peer-reviewedCC BY-NC-NDJournal of gastrointestinal oncology

FAM84B drives colon adenocarcinoma progression via stemness maintenance and tumor microenvironment remodeling.

  • Qinghua Li1
  • Zichao Cao2
  • Xiangyue Guo3
  • Hong Yu4
  • Wen Xiao1
  • Min Zhao5
  • Biaolin Zheng5
  • Zhuliang Zhang5
  • Weitao Que3,6
  • Yanzhi Jiang5
6 affiliations
  1. 1Department of Medical Oncology, Shenzhen Third People's Hospital, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen, China.
  2. 2Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  3. 3Department of Liver Surgery and Organ Transplantation Center, Shenzhen Third People's Hospital, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen, China.
  4. 4Department of Pathology, Shenzhen Third People's Hospital, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen, China.
  5. 5Department of Gastroenterology, Shenzhen Third People's Hospital, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen, China.
  6. 6Laboratory Animal Center, National Clinical Research Center for Infectious Diseases, Shenzhen, China.
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Abstract

FAM84B is oncogenic in multiple malignancies, but its precise role in colon adenocarcinoma (COAD) remains unclear. This study aims to integrate multi-omics analyses with experimental validation to elucidate the functional significance of FAM84B in COAD. FAM84B expression was analyzed using The Cancer Genome Atlas (TCGA) and single-cell RNA sequencing datasets. Cancer stemness, tumor microenvironment (TME) remodeling, and predicted drug sensitivity were evaluated bioinformatically. Key findings were validated via in vitro assays, in vivo xenografts using FAM84B-overexpressing SW480 cells, and clinical tissue microarrays (TMAs). FAM84B was significantly upregulated in COAD and robustly promoted tumor growth. Pseudotime and single-cell analyses revealed that FAM84B maintained cancer stem cell (CSC) properties, upregulating key markers [PROM1 (CD133), CD44, SOX2, POU5F1 (OCT4), and LGR5]. FAM84B orchestrated a TME phenotypic switch from an immune-engaged to a stroma-dominated state, enhanced pro-tumorigenic intercellular communication, and drove invasion via epithelial-mesenchymal transition (EMT). Furthermore, FAM84B exhibited bidirectional predicted drug sensitivity: FAM84B-high tumors displayed predicted resistance to 5-fluorouracil and oxaliplatin but predicted sensitivity to irinotecan, with the converse pattern in FAM84B-low tumors. Mechanistic networks linked FAM84B to DNA repair, angiogenesis, and drug metabolism. Western blot analysis confirmed that FAM84B overexpression upregulated c-Myc protein and p-c-Myc (Ser62) despite decreased MYC mRNA. FAM84B drives COAD progression by promoting proliferation and invasion, maintaining CSC properties, remodeling the immunosuppressive TME, and bidirectionally modulating predicted drug sensitivity. These findings establish FAM84B as a candidate prognostic biomarker and a promising therapeutic target for personalized COAD treatment.

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Cite

BibTeXRIS
BibTeX
@article{li2026fam84b,
  title = {{FAM84B drives colon adenocarcinoma progression via stemness maintenance and tumor microenvironment remodeling.}},
  author = {Qinghua Li and Zichao Cao and Xiangyue Guo and Hong Yu and Wen Xiao and Min Zhao and Biaolin Zheng and Zhuliang Zhang and Weitao Que and Yanzhi Jiang},
  journal = {Journal of gastrointestinal oncology},
  year = {2026},
  month = aug,
  doi = {10.21037/jgo-2026-0720},
  url = {https://europepmc.org/article/MED/42996561},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - FAM84B drives colon adenocarcinoma progression via stemness maintenance and tumor microenvironment remodeling.
AU  - Qinghua Li
AU  - Zichao Cao
AU  - Xiangyue Guo
AU  - Hong Yu
AU  - Wen Xiao
AU  - Min Zhao
AU  - Biaolin Zheng
AU  - Zhuliang Zhang
AU  - Weitao Que
AU  - Yanzhi Jiang
PY  - 2026
DA  - 2026/08/31
JO  - Journal of gastrointestinal oncology
DO  - 10.21037/jgo-2026-0720
UR  - https://europepmc.org/article/MED/42996561
AB  - FAM84B is oncogenic in multiple malignancies, but its precise role in colon adenocarcinoma (COAD) remains unclear. This study aims to integrate multi-omics analyses with experimental validation to elucidate the functional significance of FAM84B in COAD. FAM84B expression was analyzed using The Cancer Genome Atlas (TCGA) and single-cell RNA sequencing datasets. Cancer stemness, tumor microenvironment (TME) remodeling, and predicted drug sensitivity were evaluated bioinformatically. Key findings were validated via in vitro assays, in vivo xenografts using FAM84B-overexpressing SW480 cells, and clinical tissue microarrays (TMAs). FAM84B was significantly upregulated in COAD and robustly promoted tumor growth. Pseudotime and single-cell analyses revealed that FAM84B maintained cancer stem cell (CSC) properties, upregulating key markers [PROM1 (CD133), CD44, SOX2, POU5F1 (OCT4), and LGR5]. FAM84B orchestrated a TME phenotypic switch from an immune-engaged to a stroma-dominated state, enhanced pro-tumorigenic intercellular communication, and drove invasion via epithelial-mesenchymal transition (EMT). Furthermore, FAM84B exhibited bidirectional predicted drug sensitivity: FAM84B-high tumors displayed predicted resistance to 5-fluorouracil and oxaliplatin but predicted sensitivity to irinotecan, with the converse pattern in FAM84B-low tumors. Mechanistic networks linked FAM84B to DNA repair, angiogenesis, and drug metabolism. Western blot analysis confirmed that FAM84B overexpression upregulated c-Myc protein and p-c-Myc (Ser62) despite decreased MYC mRNA. FAM84B drives COAD progression by promoting proliferation and invasion, maintaining CSC properties, remodeling the immunosuppressive TME, and bidirectionally modulating predicted drug sensitivity. These findings establish FAM84B as a candidate prognostic biomarker and a promising therapeutic target for personalized COAD treatment.
SN  - 2078-6891
SN  - 2219-679X
ER  -