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

Zhen-Qian Qin1, Kong-Dong Li2, He-Zhen Chu3

  • 1Affiliated Hospital of Jiangsu University-Yixing Hospital, Yixing, Jiangsu, China.

Neoplasma
|December 9, 2021
PubMed

Insights

High stanniocalcin 2 (STC2) expression promotes sunitinib resistance in kidney cancer. Targeting STC2 with antibodies may overcome this resistance, offering a new immunotherapy approach for clear cell renal cell carcinoma (ccRCC).

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Stanniocalcin 2 (STC2) is a prognostic marker in renal cell carcinoma, but its precise role remains unclear.
  • Elevated STC2 expression is observed in kidney renal clear cell carcinoma (KIRC).

Purpose of the Study:

  • To investigate the association between high STC2 expression and sunitinib resistance in clear cell renal cell carcinoma (ccRCC).
  • To elucidate the underlying mechanisms of STC2-mediated sunitinib resistance.

Main Methods:

  • Analysis of TCGA database using the GEPIA platform.
  • Real-time quantitative PCR and Western blotting to assess STC2 expression.
  • Enzyme-linked immunosorbent assay (ELISA) for STC2 secretion.
  • In vitro experiments using ccRCC cells with STC2 neutralizing antibodies and recombinant STC2.

Main Results:

  • STC2 expression and secretion were significantly higher in ccRCC cells compared to normal renal cells.
  • STC2 neutralizing antibodies reduced sunitinib resistance, while recombinant STC2 aggravated it.
  • Sunitinib treatment decreased STC2 expression and secretion, disrupted lysosomal pH, and led to intracellular accumulation.
  • STC2 antibody treatment reduced sunitinib accumulation, enhancing its anti-proliferative effects.

Conclusions:

  • STC2 plays a crucial role in promoting sunitinib resistance in ccRCC.
  • STC2 represents a potential therapeutic target for ccRCC treatment.
  • Anti-STC2 antibodies may offer a future immunotherapy strategy for ccRCC.

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