ArticleFrontiers in oncology2022
SEMA3C Supports Pancreatic Cancer Progression by Regulating the Autophagy Process and Tumor Immune Microenvironment.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Biomarker-Driven Strategies for Stromal Reprogramming in Pancreatic Ductal Adenocarcinoma.Cells · 2026Review
- Regenerative macrophages enhance stem cell-derived β cell function and engraftment.Science advances · 2026Article
- A LINE-1 retrotransposon promotes SEMA3C expression as a cis-regulatory enhancer to sustain breast cancer stem cell survival.Science China. Life sciences · 2026Article
- Single-nucleus RNA sequencing reveals the effects of key regulators on human pancreatic adenocarcinoma and its tumor microenvironment.Journal of gastrointestinal oncology · 2026Article
- The SOX4-Semaphorin3C axis promotes esophageal adenocarcinoma progression.Cancer letters · 2025Article
- Baicalin Alleviates Piglet Immunosuppression Induced byBiomolecules · 2025Article
- Clustering Analysis of Multiple Omics Data Types Identifies Cancer Patients With Consistent Survival Outcomes.Cancer informatics · 2025Article
- Article
- Semaphorin3C identified as mediator of neuroinflammation and microglia polarization after spinal cord injury.iScience · 2024Article
- Characterization of the malignant cells and microenvironment of infantile fibrosarcoma via single-cell RNA sequencing.Translational pediatrics · 2024Article
- Article
- Molecular profile of metastasis, cell plasticity and EMT in pancreatic cancer: a pre-clinical connection to aggressiveness and drug resistance.Cancer metastasis reviews · 2024Review
- Integrated bioinformatics analysis of SEMA3C in tongue squamous cell carcinoma using machine-learning strategies.Cancer cell international · 2024Article
- Metabolic reprogramming, autophagy, and ferroptosis: Novel arsenals to overcome immunotherapy resistance in gastrointestinal cancer.Cancer medicine · 2023Review
- Modulation of semaphorin 3C & 4D expression in cancerous tissues from individuals with laryngeal squamous cell carcinoma.The Indian journal of medical research · 2023Article
- Semaphorin 3 C enhances putative cancer stemness and accelerates peritoneal dissemination in pancreatic cancer.Cancer cell international · 2023Article
- Proteomic profiling of gastric cancer with peritoneal metastasis identifies a protein signature associated with immune microenvironment and patient outcome.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023Article
- Article
- Semaphorins and their receptors in pancreatic cancer: Mechanisms and therapeutic opportunities.Frontiers in oncology · 2022Review
- Interplay of four types of RNA modification writers revealed distinct tumor microenvironment and biological characteristics in pancreatic cancer.Frontiers in immunology · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
To date, driver genes for pancreatic cancer treatment are difficult to pursue therapeutically. Targeting mutated KRAS, the most renowned driver gene in pancreatic cancer, is an active area of study. We discovered a gene named SEMA3C was highly expressed in pancreatic cancer cell lines and patients with a G12D mutation in KRAS. High expression of SEMA3C in patients was significantly associated with the decreased survival of pancreatic cancer patients based on the TCGA database. In pancreatic cancer cells, SEMA3C knockdown or inhibition exhibited growth/colony inhibition and cell cycle arrest. In addition, SEMA3C inhibition sensitized KRAS or MEK1/2 inhibition in pancreatic cancer cells. Overexpression of SEMA3C resulted in the induction of autophagy, whereas depletion of SEMA3C compromised induction of autophagy. SEMA3C modified the PD-L1 expression in tumor and immune cells and is correlated with the M2-like macrophage marker ARG1/CD163 expression, which could reshape the tumor microenvironment. Inhibition of SEMA3C decreased tumor formation in the xenograft model
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