Background: TCIRG1, also known as V-ATPase-a3, is critical for cellular life activities through its dependent acidification. Prior to the present research, its relationship with prognostic and tumor immunity in clear cell renal cell carcinoma (ccRCC) had not yet been investigated. Methods: We assessed TCIRG1 expression in normal and tumor tissues using data from TCGA, GEO, GTEX, and IHC. We also analyzed the relationship between TCIRG1 and somatic mutations, TMB, DNA methylation, cancer stemness, and immune infiltration. We evaluated the relevance of TCIRG1 to immunotherapy and potential drugs. Finally, we explored the effect of TCIRG1 knockdown on tumor cells. Results: TCIRG1 was overexpressed in tumor tissue and predicted a significantly unfavorable clinical outcome. High TCIRG1 expression may be associated with fewer PBRM1 and more BAP1 mutations and may reduce DNA methylation, thus leading to a poor prognosis. TCIRG1 was strongly associated with CD8+ T-cell, Treg, and CD4+ T-cell infiltration. Moreover, TCIRG1 was positively correlated with TIDE scores and many drug sensitivities. Finally, experiments showed that the knockdown of TCIRG1 inhibited the migration of ccRCC cells. Conclusions: TCIRG1 may have great potential in identifying prognostic and immunomodulatory mechanisms in tumor patients and may provide a new therapeutic strategy for ccRCC.

Cuproptosis, a newly discovered programmed cell death induced by copper ions, is associated with the progression and drug resistance of various tumors. Docetaxel plays a vital role as a first‐line chemotherapeutic agent for advanced prostate cancer; however, most patients end up with prostate cancer progression because of inherent or acquired resistance. Herein, we examined the role of cuproptosis in the chemotherapeutic resistance of prostate cancer to docetaxel. We treated prostate cancer cell lines with elesclomol–CuCl2, as well as with docetaxel. We performed analyses of CCK8, colony formation tests, cell cycle flow assay, transmission electron microscopy, and mTOR signaling in treated cells, and treated a xenograft prostate cancer model with elesclomol–CuCl2 and docetaxel in vivo, and performed immunohistochemistry and Western blotting analysis in treated tumors. We found that elesclomol–CuCl2 could promote cell death and enhance chemosensitivity to docetaxel. Elesclomol–CuCl2 induced cell death and inhibited the growth of prostate cancer cells relying on copper ions‐induced cuproptosis, not elesclomol. In addition, dihydrolipoamide S‐acetyltransferase (DLAT) was involved in cuproptosis‐enhanced drug sensitivity to docetaxel. Mechanistically, upregulated DLAT by cuproptosis inhibited autophagy, promoted G2/M phase retention of cells, and enhanced the sensitivity to docetaxel chemotherapy in vitro and in vivo via the mTOR signaling pathway. Our findings demonstrated that the cuproptosis‐regulated DLAT/mTOR pathway inhibited autophagy and promoted cells in G2/M phase retention, thus enhancing the chemosensitivity to docetaxel. This discovery may provide an effective therapeutic option for treating advanced prostate cancer by inhibiting the chemotherapeutic resistance to docetaxel.

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Background Venous tumor thrombus is one of the clinical features of progressive kidney cancer, causing a low 5-year survival rate. The current best treatment method is still complete resection of renal and venous tumor thrombus through surgery, which can effectively improve the prognosis of patients. The mainstream surgical methods include open surgery and minimally invasive surgery, but most of them require intraoperative position change to achieve the purpose of complete resection of venous tumor thrombus. Case presentation A 54-year-old woman was found to have a left kidney tumor by accident. Further examination showed that the left renal vein was invaded, and the inferior vena cava had not invaded. The patient had no clinical symptoms, and no obvious abdominal mass was found on physical examination. The surgery was performed using a single position, 4-hole transabdominal laparoscopic technique. The patient recovered well after the operation and was discharged from the hospital 4 days later. The postoperative pathology was: clear cell carcinoma grade III with hemorrhagic necrosis. We prescribed oral sorafenib mesylate tablets 400mg/day after discharge. After 6 months of follow-up, there was no recurrence or metastasis, and the patient recovered well. Conclusion Single position with 4-hole laparoscopic radical nephrectomy and tumor thrombectomy is safe and feasible for low-grade venous tumor thrombus. It has the advantages of simple operation steps, less trauma, quick postoperative recovery, fewer complications, worthing clinical application, and promotion.