NR6A1 (Nuclear Receptor Subfamily 6 Group A Member 1)

Together, these findings identify the SPACA6-hosted miR-99b~125a~let-7e cluster as a regulator of BRAF/MEK inhibitor resistance through promotion of tumor survival and of an immunosuppressive microenvironment. Targeting this miRNA cluster may provide novel therapeutic opportunities to overcome drug resistance in metastatic melanoma.

In addition, we found that NR6A1 can affect mTOR signaling, suggesting a broader role in tumor metabolism regulation. In summary, our data indicate that NR6A1 plays an oncogenic role by reprogramming glycolysis via the miR-302a/HK1 axis in lung adenocarcinoma.

Subsequently, S100A4 upregulates p53 expression, thereby promoting AML cell proliferation and resistance to Ara-C. In summary, our comprehensive investigation of the ARRGRS not only deepens the understanding of Ara-C resistance mechanisms but also provides promising insights for targeting S100A4 to inhibit tumor growth and overcome chemotherapy resistance in AML.

Furthermore, EGFR tyrosine kinase inhibitors may suppress metastasis in these contexts. This study provides novel insights into the oncogenic role of Lm-γ2F in NSCLC, highlighting its potential as a therapeutic target to mitigate tumor progression and metastasis.

[This retracts the article on p. 114 in vol. 14, PMID: 38323281.].

Different novel targets were found, in particular ARID3A, CCNJ, LIPA, NR6A1, and NUP210, oncogenes in various tumors and here also related to HCC through miR-125a regulation. The RNA interactions investigated in this work could pave the way to piece together the RNA regulatory networks governed by the miRNA impacting on hepatocarcinogenesis, and be exploited in the future for identifying novel biomarkers and therapeutic targets in HCC.

Previously, we identified that resistance to tamoxifen and rapamycin is associated with the suppression of DNMT3A. The coordinated suppression of NR6A1 and DNMT3A may contribute to sustaining the resistant phenotype in breast cancer cells. This pathway could serve as a predictive marker, helping guide the selection of optimal therapeutic strategies for breast cancer treatment in the future.

More significantly, this study provides valuable insight into potential references for systemic antitumor immunity of ablation against low-risk thyroid cancer. This trial is registered with ChiCTR1900024544.

10-gene signature also further categorized patients classified as molecular subtypes according to risk scores. Our novel findings may help address the prognostic challenges in TNBC and the 10-gene signature could serve as a novel biomarker for risk-based patient care.

Moreover, the overexpression of the miR-99b/let-7e/miR-125a cluster inhibited liver metastases and tumor formation. Thus, the study concludes that the miR-99b/let-7e/miR-125a cluster impedes the invasion and metastasis of PCa cells via targeting the NR6A1 gene.

In summary, histone Kla was related to HCC prognosis and might serve as an independent biomarker. NR6A1, OSBP2 and UNC119B were associated with the prognosis, immunotherapy, and chemotherapy resistance, suggesting that NR6A1, OSBP2 and UNC119B might be novel candidate therapeutic targets for HCC.

Finally, let-7a-5p abrogates PCT xenograft tumors growth, NR6A1 expression and lipogenesis. Taken together, our data indicates that let-7a-5p suppresses PCT progression through decreased lipogenesis, the related let-7a-5p/NR6A1axis might be promising candidate targets for PTC treatment.