New Ca based anticancer nanomaterials trigger multiple cell death targeting Ca homeostasis for cancer therapy.

Calcium ion (Ca) is a necessary element for human and Ca homeostasis plays important roles in various cellular process and functions. Recent reaches have targeted on inducing Ca overload (both intracellular and transcellular) for tumor therapy. With the development of nanotechnology, nanoplatform-mediated Ca overload has been safe theranostic model for cancer therapy, and defined a special calcium overload-induced tumor cell death as "calcicoptosis".

Inhibiting stanniocalcin 2 reduces sunitinib resistance of Caki-1 renal cancer cells under hypoxia condition.

Background: Our previous study has suggested that blocking stanniocalcin 2 (STC2) could reduce sunitinib resistance in clear cell renal cell carcinoma (ccRCC) under normoxia. The hypoxia is a particularly important environment for RCC occurrence and development, as well as sunitinib resistance. The authors proposed that STC2 also plays important roles in RCC sunitinib resistance under hypoxia conditions.

Calcium-Sensing Receptor (CaSR)-Mediated Intracellular Communication in Cardiovascular Diseases.

The calcium-sensing receptor (CaSR), a G-protein-coupled receptor (GPCR), is a cell-surface-located receptor that can induce highly diffusible messengers (IP3, Ca, 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.

Blocking stanniocalcin 2 reduces sunitinib resistance in clear cell renal cell carcinoma.

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.