STRA6 (Signaling Receptor And Transporter Of Retinol STRA6)

This study identifies ARNT2 as a transcriptional modulator of fatty acid metabolism pathways, highlighting its potential as a viable molecular target for RLPS therapy.

The paper provides experimental support for the theoretical hypothesis of how retinoic acid catalyzes resonance energy transfer reactions and controls the activation/inactivation cycle of protein kinase PKCδ. It has been proposed that reversible phosphorylation of cytochrome c mediated by cell signaling pathways is a primary regulatory mechanism that determines mitochondrial respiration, electron transport chain (ETC) flux, proton gradient ΔΨm, ATP production, and ROS generation, linking oxidative phosphorylation to human cancer through a lack of energy, ROS production, cytochrome c release, and activation of apoptosis.

Our study uncovers a novel STRA6/STAT3/SREBP-1 regulatory axis that enhances NSCLC metastasis by reprogramming of lipid metabolism. These results demonstrate the potential use of STRA6 as a biomarker for diagnosing NSCLC, which may therefore potentially serve as a therapeutic target for NSCLC.

In conclusion, we demonstrate that VIRMA can increase glycolysis in PDAC by upregulating STRA6, a cell surface membrane protein that stimulates the STAT3 pathway, thereby activating HIF-1α and leading to pancreatic cancer malignancy. Overall, our data strongly suggest that the VIRMA-STRA6-STAT3-HIF-1α axis is a viable therapeutic target in PDAC.

There is extreme heterogeneity of epithelial cells in HGSOC, and STRA6+ granulosa cells may be able to promote cancer progression. Our findings are benefit to the heterogeneity identification of HGSOC and develop targeted therapy strategy for HGSOC patients.

We further confirmed that ANLN could upregulate STRA6 expression, which activated PI3K/AKT signaling to enhance the growth and movement of GBC cells. These findings demonstrate ANLN's involvement in GBC initiation and progression, suggesting its potential as a novel target for GBC.

Additionally, we discovered that STRA6 suppresses apoptosis partly by controlling BCL2 expression, which in turn causes CRC to become resistant to LOHP treatment. Our study demonstrates that STRA6 is a potential prognostic factor and oncogene in CRC by promoting CRC growth and chemoresistance.

Moreover, STRA6 promoted epithelial-mesenchymal transition via increased cancer-associated fibroblasts infiltration. Our study demonstrates STRA6 may serve as a prognostic marker for BRAF-mutated PTC, which may drive thyroid carcinogenesis via activation of oncogenic pathway and regulation of tumor immunosuppressive microenvironment.

Our study demonstrates the critical roles of STRA6 contributing to TC progression via the ILK/AKT/mTOR axis, which may provide a novel prognostic marker as well as a promising therapeutic target for aggressive TC.