ArticleJournal of translational medicine2024
The SIX2/PFN2 feedback loop promotes the stemness of gastric cancer cells.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- MRPL13 sustains mitochondrial integrity and MAPK-associated aggressiveness in esophageal squamous cell carcinoma.Cancer cell international · 2026Article
- Profilin and Its Isoforms: Unravelling the Functional Diversity Across Life Forms.Current protein & peptide science · 2026Review
- TRIM21-mediated ubiquitination of SIX2 attenuates breast cancer stemness via LGSN suppression.Oncogene · 2025Article
- Targeting SIX2 as a novel sensitization strategy of sorafenib treatment on advanced hepatocellular carcinoma through modulating METTL9-SLC7A11 axis.NPJ precision oncology · 2025Article
- A Multi-Faceted Approach to Explore the Role of Inflammatory CAFs, Providing Prognostic Value and Therapeutic Implications in Lung Adenocarcinoma.International journal of genomics · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundThe roles of the transcriptional factor SIX2 have been identified in several tumors. However, its roles in gastric cancer (GC) progression have not yet been revealed. Our objective is to explore the impact and underlying mechanisms of SIX2 on the stemness of GC cells.
methodsLentivirus infection was employed to establish stable expression SIX2 or PFN2 in GC cells. Gain- and loss-of-function experiments were conducted to detect changes of stemness markers, flow cytometry profiles, tumor spheroid formation, and tumor-initiating ability. ChIP, RNA-sequencing, tissue microarray, and bioinformatics analysis were performed to reveal the correlation between SIX2 and PFN2. The mechanisms underlying the SIX2/PFN2 loop-mediated effects were elucidated through tissue microarray analysis, RNA stability assay, IP-MS, Co-Immunoprecipitation, and inhibition of the JNK signaling pathway.
resultsThe stemness of GC cells was enhanced by SIX2. Mechanistically, SIX2 directly bound to PFN2's promoter and promoted PFN2 activity. PFN2, in turn, promoted the mRNA stability of SIX2 by recruiting RNA binding protein YBX-1, subsequently activating the downstream MAPK/JNK pathway.
conclusionThis study unveils the roles of SIX2 in governing GC cell stemness, defining a novel SIX2/PFN2 regulatory loop responsible for this regulation. This suggests the potential of targeting the SIX2/PFN2 loop for GC treatment (Graphical Abstracts).
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