ArticleiScience2021
Arl4c promotes the growth and drug resistance of pancreatic cancer by regulating tumor-stromal interactions.
Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Implications of ADP-Ribosylation Factor-Like Protein 4C (ARL4C) in Human Neoplasia With Special Emphasis on Ameloblastoma: A Scoping Review.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026Article
- Sex-related differences in gene expression in early-stage bladder cancer revealed by whole-transcriptome sequencing.BMC cancer · 2026Article
- Pancreatic stellate cells: Key players in pancreatic health and diseases (Review).Molecular medicine reports · 2024Review
- Prognostic stratification of sepsis through DNA damage response based RiskScore system: insights from single-cell RNA-sequencing and transcriptomic profiling.Frontiers in immunology · 2024Article
- Identification of a Novel Mesenchymal Stem Cell-Related Signature for Predicting the Prognosis and Therapeutic Responses of Bladder Cancer.Stem cells international · 2024Article
- Determinants of gemcitabine response in pancreatic cancer: are we there?Journal of gastrointestinal oncology · 2023Article
- Comprehensive Analyses of Stromal-Immune Score-Related Competing Endogenous RNA Networks In Colon Adenocarcinoma.Disease markers · 2022Article
- ARL4C Regulates the Progression of Clear Cell Renal Cell Carcinoma by Affecting the Wnt/Journal of oncology · 2022Article
- CircRNAs in Pancreatic Cancer: New Tools for Target Identification and Therapeutic Intervention.Cancer genomics & proteomicsReview
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence suggests that ADP-ribosylation factor like-4c (Arl4c) may be a potential choice for cancer treatment. However, its role in pancreatic cancer, especially in tumor-stroma interactions and drug resistance, is still unknown. In the current study, we examined the proliferation and drug resistance effect of Arl4c on pancreatic cancer cells. Furthermore, we explored the contribution of Arl4c high expression in pancreatic stellate cell (PSC) activation. We found that high Arl4c expression is associated with cell proliferation, drug resistance, and PSC activation. In detail, Arl4c regulates connective tissue growth factor (CTGF) paracrine, further induces autophagic flux in PSCs, resulting in PSC activation. TGFβ1 secreted by activated PSCs enhances cancer cell stem cell properties via smad2 signaling, further increasing cell drug resistance. YAP is an important mediator of the Arl4c-CTGF loop. Taken together, these results suggest that Arl4c is essential for pancreatic cancer progression and may be an effective therapeutic choice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.