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Peer-reviewedCC BYBMC cancer

Transcriptomic profiling reveals autophagy-associated programs and prognostic biomarkers in anoikis-resistant pancreatic cancer cells.

  1. 1Department of Breast Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
  2. 2Department of Surgery, Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden.
  3. 3Department of Surgery, Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden. [email protected].

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is characterized by aggressive metastatic progression and poor clinical outcomes. During metastatic dissemination, detached tumor cells must overcome anoikis, a form of apoptosis induced by loss of extracellular matrix attachment. Although anoikis resistance is considered a critical prerequisite for metastasis, the adaptive mechanisms supporting detached survival in pancreatic cancer remain incompletely understood. In this study, anoikis-resistant (AR) pancreatic cancer cell models were established through repeated long-term suspension culture using Capan-1 and PSN-1 cells. Transcriptomic profiling was performed to identify conserved molecular programs associated with anoikis resistance in PDAC. Gene set variation analysis (GSVA) demonstrated consistent transcriptomic enrichment of autophagy-associated and suppression of cell cycle-related pathways in both AR models. Differential expression and integrative pathway analyses further identified several core genes associated with autophagy regulation and cytokine signaling. Survival analysis revealed that elevated expression of UBC and ATG14 was associated with poor prognosis in pancreatic cancer patients. Our findings suggest that suspension-selected pancreatic cancer cells undergo coordinated stress-adaptive transcriptional remodeling characterized by enriched autophagy- and ubiquitin-associated transcriptional programs.

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BibTeX
@article{lin2026transcriptomic,
  title = {{Transcriptomic profiling reveals autophagy-associated programs and prognostic biomarkers in anoikis-resistant pancreatic cancer cells.}},
  author = {Lizhi Lin and Monika Bauden and Roland Andersson and Daniel Ansari},
  journal = {BMC cancer},
  year = {2026},
  month = oct,
  doi = {10.1186/s12885-026-17107-7},
  url = {https://europepmc.org/article/MED/42888392},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Transcriptomic profiling reveals autophagy-associated programs and prognostic biomarkers in anoikis-resistant pancreatic cancer cells.
AU  - Lizhi Lin
AU  - Monika Bauden
AU  - Roland Andersson
AU  - Daniel Ansari
PY  - 2026
DA  - 2026/10/13
JO  - BMC cancer
DO  - 10.1186/s12885-026-17107-7
UR  - https://europepmc.org/article/MED/42888392
AB  - Pancreatic ductal adenocarcinoma (PDAC) is characterized by aggressive metastatic progression and poor clinical outcomes. During metastatic dissemination, detached tumor cells must overcome anoikis, a form of apoptosis induced by loss of extracellular matrix attachment. Although anoikis resistance is considered a critical prerequisite for metastasis, the adaptive mechanisms supporting detached survival in pancreatic cancer remain incompletely understood. In this study, anoikis-resistant (AR) pancreatic cancer cell models were established through repeated long-term suspension culture using Capan-1 and PSN-1 cells. Transcriptomic profiling was performed to identify conserved molecular programs associated with anoikis resistance in PDAC. Gene set variation analysis (GSVA) demonstrated consistent transcriptomic enrichment of autophagy-associated and suppression of cell cycle-related pathways in both AR models. Differential expression and integrative pathway analyses further identified several core genes associated with autophagy regulation and cytokine signaling. Survival analysis revealed that elevated expression of UBC and ATG14 was associated with poor prognosis in pancreatic cancer patients. Our findings suggest that suspension-selected pancreatic cancer cells undergo coordinated stress-adaptive transcriptional remodeling characterized by enriched autophagy- and ubiquitin-associated transcriptional programs.
SN  - 1471-2407
ER  -