IGHG1 promotes motility likely through epithelial-mesenchymal transition in ovarian cancer

Objective： Ovarian cancer（OC） is one of the leading causes of death for female cancer patients. COC166-9 is an OC-specific monoclonal antibody and we have identified immunoglobulin γ-1 heavy chain constant region（IGHG1） as its antigen. We explore the function of IGHG1 in proliferation, apoptosis and motility of OC cells further in this research.Methods： IGHG1 expression in OC specimens was detected through immunohistochemistry. Real-time quantitative polymerase chain reaction（RT-q PCR） or western blotting assay was used to test IGHG1 expression in OC cells. Viability of OC cells was tested by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide（MTT）assay. Flow cytometry or western blotting assay was used to detect cell cycle and apoptosis. Cellular motility was analyzed by using transwell assay and the markers of epithelial-mesenchymal transition（EMT） were tested through immunoblots.Results： Although it exerts negligible effect on the viability and apoptosis of OC cells, IGHG1 could promote migration and invasion of malignant cells in vitro. Mechanistically, IGHG1 increases the expression of N-cadherin and Vimentin while decreases E-cadherin expression. Additionally, IGHG1 expression in OC specimens is higher relative to the paired normal counterparts. Further analysis demonstrates that the increased IGHG1 expression correlates positively with the lymph node metastasis of OC.Conclusions： IGHG1 promotes the motility of OC cells likely through executing the EMT program. Increased IGHG1 expression in OC specimens is associated with the lymph node metastasis.

Aiphanol, a native compound, suppresses angiogenesis via dual-targeting VEGFR2 and C0X2

Dear Editor,Pathological neo-vascularization is a hallmark of cancer and several diseases.Accumulating evidence supports the notion that antiangiogenic treatment can abolish tumor angiogenesis to achieve Ion ger disease-free survival.Although growth factors and their receptors function as the main drivers in angiogenesis,the involvement of other regulators,e.g.,Cyclooxygenase-2(COX2),^(1) should also be con sidered,especially for managi ng the resista nee to therapies against receptor tyrosine kinases(RTKs).

Correction: Aiphanol, a native compound, suppresses angiogenesis via dual-targeting VEGFR2 and COX2

Correction to:Signal Transduction and Targeted Therapy https://doi.org/10.1038/s41392-021-00739-5,published online 03 December 2021 After online publication of the letter1,the author found two images in the supplement materials were used incorrectly,Additionally,there is an error in the chemical structure of Aiphanol in Figs.1a and 1s that needs to be corrected.The correct data are provided as follows.The key findings of the article are not affected by these corrections.The original article has been corrected.