Rptor, also known as regulatory associated protein of MTOR complex 1, is a key component of the mTORC1 pathway. The mTORC1 pathway is central in promoting growth in response to insulin, energy levels, and amino acids, and is often deregulated in cancers. Rptor plays a role in various biological processes, with its function being studied through genetic models to understand its importance in normal and disease-related conditions [3,5].

In esophageal squamous cell carcinoma (ESCC), METTL1 or WDR4 knockdown leads to decreased expression of m7G-modified tRNAs, reducing the translation of a subset of oncogenic transcripts enriched in the RPTOR/ULK1/autophagy pathway. Mettl1 conditional knockout and knockin mice models demonstrate the essential function of METTL1 in promoting ESCC tumorigenesis, suggesting that Rptor in this axis may be a potential therapeutic target [1].

In NSCLC brain metastasis, RPTOR was significantly upregulated in BM foci, and RPTOR blockade in xenograft and zebrafish models suppressed BM by interfering with ceramide metabolism, indicating its role as a key driver gene [2].

In melanoma, RPTOR-mutation patients had prolonged overall survival and a higher objective response rate to immune checkpoint inhibitors compared to RPTOR-wildtype patients, suggesting RPTOR mutation could be a predictor of effective immunotherapy [4].

In conclusion, Rptor is crucial in the mTORC1 pathway and plays significant roles in multiple disease conditions. Studies using gene knockout or conditional knockout mouse models have revealed its importance in cancer-related processes such as tumorigenesis, metastasis, and response to immunotherapy, providing insights for potential therapeutic strategies in these diseases.