NR2C2 (Nuclear Receptor Subfamily 2 Group C Member 2)

Mirin suppressed lymph node metastasis of PCa cells in vivo. Our study demonstrated a novel function of the YEATS2/NR2C2/RAD50 axis in regulating DNA damage responses and anoikis resistance in PCa metastasis, highlighting an important pathway that drives metastatic progression and offering potential new strategies for treating mPCa.

Furthermore, the preclinical investigation demonstrated that targeting this newly identified signaling with lipofermata (a FATP2-specific inhibitor) suppressed PTC progression. Together, these findings suggest that adipocytes in the PTC microenvironment may function via FATP2/TR4 signaling to regulate PTC progression, and targeting this newly identified adipocyte/FATP2/TR4 signaling axis may facilitate the development of novel therapeutic strategies for PTC.

Crucially, the re-expression of ARPC1B in NAA30-silenced cells effectively restored these malignant phenotypes. These findings highlight the critical role of the NR2C2-NAA30-ARPC1B axis in ovarian cancer progression and provide more foundation for the development of more effective treatment strategies for patients with ovarian cancer.

Functionally, knockdown of ALKBH1 increases NR2C2 expression, leading to decreased mTOR activation and global translation. Our work uncovers a previously unknown mechanism into arsenic tumorigenicity, adds understanding into the functional effect of arsenic binding to proteins, and implicates ALKBH1 as a potential druggable target and biomarker for arsenic tumorigenicity.

Furthermore, ASCC3 may regulate tumor immunity by affecting T cell function. ASCC3 can serve as an independent prognostic factor for READ and can synergize with various immune-related genes to influence patient prognosis.

Our study reveals an expanded FOXA1 interactome and new insights into its functional network in breast cancer, providing candidate proteins for further exploration as biomarkers or therapeutic targets. Implications: These findings expand the FOXA1 interactome in breast cancer and uncover new candidate proteins with potential as biomarkers and therapeutic targets in hormone-driven tumors.

Moreover, elevated DDX41 levels increase liver cancer cell sensitivity to protein synthesis inhibitors; treatment with homoharringtonine (HHT), an approved drug, significantly inhibits tumor growth in DDX41-overexpressing liver cancer models. Taken together, the results of this study highlight that DDX41 acts as an oncogene in liver cancer and suggest that protein synthesis inhibition may be a promising therapy for liver cancers with high DDX41 expression.

Thus, nuclear receptors serve as novel targets for tumor radiosensitization and for protecting of normal tissues from radiation damage. This review summarizes the research progress of nuclear receptors and highlights a promising synergistic strategy in radiotherapy.

Alterations induced by KMT5C knockdown were partly reversed by UPP1 inhibition. Overall, we demonstrate that KMT5C, recruited by NR2C2, suppresses OSCC progression by inhibiting UPP1 transcription in a H4K20me3-dependent way.

Nr2e3 knockdown decreased the mRNA and protein expression levels of nr2c2, whereas nr2c2 overexpression reversed the elevated CD44CD24 cell ratio and the increased migratory activity caused by nr2e3 silencing. The results of the present study suggest that NR2E3 may serve an important role in modulating the stem-like properties of ER breast cancer cells, where NR2E3/NR2C2 signaling may be a therapeutic target in ER breast cancer.

This study identifies that miR-616-5p can promote bladder cancer progression via altering the expression of NR2C2. Therefore, identifying miR-616-5p expression levels might be a useful strategy for developing potential therapeutic targets in bladder cancer.

Moreover, TR4 mice showed a lower grade of histopathology than the control group. In conclusion, these results indicate that TR4 plays a key role in bladder cancer proliferation, and targeting TR4 would probably be a potential strategy for bladder cancer treatment.