ArticleAmerican journal of cancer research2026
Unc-51 like kinase 3 induces reticulophagy by mediating the GLI1/CAMK2B signaling pathway to promote the malignant progression of prostate cancer.
Article in American journal of cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Recent studies have found that the reticulophagy pathway is able to clear excess endoplasmic reticulum to protect cells from endoplasmic reticulum stress-induced damage. The role of reticulophagy in prostate cancer is still unknown. Key genes of reticulophagy were studied. Subsequently, the ULK3 and CAMK2B mRNA levels were confirmed. ULK3 and CAMK2B expression were elevated in prostate cancer tissues. The silencing of ULK3 inhibited prostate cancer cell vitality. The overexpression of ULK3 had the opposite effect. ULK3 was able to enhance the CAMK2B protein expression by promoting the entry of GLI1 into the nucleus, thereby upregulating the level of reticulophagy. Knockdown of CAMK2B could inhibit reticulophagy induced by ULK3. Further experiments showed that ULK3 phosphorylated GLI1, promoted its nuclear entry and binding to the CAMK2B promoter to enhance CAMK2B expression. Down-regulation of ULK3 inhibited the growth of prostate cancer vitality in vivo. This study confirmed that ULK3 promoted the prostate cancer by upregulating GLI1/CAMK2B-induced reticulophagy.
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