Stanniocalcin 2 (STC2) has been identified as a prognostic marker in renal cell carcinoma.However, the role of STC2 in renal cell carcinoma is still unclear. In this study, we investigated the relationship between high expression of STC2 and sunitinib resistance in cells and the underlying mechanism. Through GEPIA platform analysis based on the TCGA database, it showed that the expression of STC2 in kidney renal clear cell carcinoma (KIRC) was significantly higher than that in the normal population. Real-time quantitative PCR and western blotting detected significantly higher expression levels of STC2 in clear cell renal cell carcinoma (ccRCC) cells than that in normal renal cells. Enzyme-linked immunosorbent assay (ELISA) determined whether there is a high secretion of STC2 in ccRCC cells. The sunitinib resistance could be significantly reduced by STC2 neutralizing antibody but aggravated by the addition of recombinant human STC2 in ccRCC cells. Sunitinib suppressed STC2 expression and secretion, destroyed lysosomal acidic pH, and accumulated in the cells. However, STC2 neutralizing antibody can reduce the accumulation of sunitinib in cells to improve the inhibitory efficiency of sunitinib on cell proliferation. This study suggested STC2 could serve as a potential novel target for the treatment of ccRCC, anti-STC2 antibody might be an option of immunotherapy in the future.
The calcium-sensing receptor (CaSR), a G-protein-coupled receptor (GPCR), is a cell-surface-located receptor that can induce highly diffusible messengers (IP3, Ca2+, cAMP) in the cytoplasm to activate various cellular responses. Recently, it has also been suggested that the CaSR mediates the intracellular communications between the endoplasmic reticulum (ER), mitochondria, nucleus, protease/proteasome, and autophagy–lysosome, which are involved in related cardiovascular diseases. The complex intracellular signaling of this receptor challenges it as a valuable therapeutic target. It is, therefore, necessary to understand the mechanisms behind the signaling characteristics of this receptor in intracellular communication. This review provides an overview of the recent research progress on the various regulatory mechanisms of the CaSR in related cardiovascular diseases and the heart–kidney interaction; the associated common causes are also discussed.
Prostate cancer is most prevalent malignancy of males in the world. In recent years, long non-coding RNAs (lncRNAs) were identified, and their functions are associated with prostate cancer initiation and progression. However, their molecular mechanisms still need to be elucidated before the clinical utility. In the present study, we identified the correlation of lncRNA inactivation escape 1 (INE1) with the characterization in prostate cancer patients, and detected the roles of INE1 in cell autophagy and apoptosis in prostate cancer cells. Our results showed that the lncRNA INE1 expression highly correlate with patients’ survival times, tumor stage, biochemical recurrence, disease recurrence and Gleason pattern. High expression of INE1 was detected in prostate cancer cells, and knockdown INE1 by siRNA resulted in significant inhibition of cell viability. In addition, silencing INE1 induced early autophagy and pro-apoptosis, which augments cisplatin (CDDP)-induced cell apoptosis. Moreover, INE1 played an anti-apoptotic role by targeting the serine/arginine-rich splicing factor 2 (SRSF2).
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