Erratum: RPL32 Promotes Lung Cancer Progression by Facilitating p53 Degradation.

[This corrects the article DOI: 10.1016/j.omtn.

Estrogen Receptor Downregulates Expression of PD-1/PD-L1 and Infiltration of CD8 T Cells by Inhibiting IL-17 Signaling Transduction in Breast Cancer.

The relationship between the interleukin 17 (IL-17) family of cytokines and breast cancer has been widely studied in recent years. Many studies have revealed increased levels of the cytokine IL-17A in estrogen receptor (ER)-negative or triple-negative breast cancer. Upregulation of IL-17A signaling is associated with increased expression of programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1) in breast cancer with low ER expression and may elevate the infiltration of CD8 T cells in tumor tissue.

RPL32 Promotes Lung Cancer Progression by Facilitating p53 Degradation.

Lung cancer is the leading cause of cancer death worldwide, and the overall survival rate of advanced lung cancer patients is unsatisfactory. Ribosomal proteins (RPs) play important roles in carcinogenesis. However, the role of RPL32 in lung cancer has not been demonstrated.

Selective capture of mesenchymal stem cells over fibroblasts and immune cells on E7-modified collagen substrates under flow circumstances.

Recruitment of endogenous mesenchymal stem cells (MSCs) has become an attractive strategy for in situ tissue regeneration. However, it is of great importance to endow an implant with a specific affinity to MSCs, for many types of cells such as immune cells and fibroblasts can also be recruited. It has been demonstrated that E7 peptides have a specific affinity to MSCs, but their selectivity for MSCs when co-cultured with other cells, especially in flow conditions, has rarely been investigated.