Erratum: PFKFB4 promotes angiogenesis via IL-6/STAT5A/P-STAT5 signaling in breast cancer: Erratum.

[This corrects the article DOI: 10.7150/jca.66773.

PTPN2 in the Immunity and Tumor Immunotherapy: A Concise Review.

PTPN2 (protein tyrosine phosphatase non-receptor 2), also called TCPTP (T cell protein tyrosine phosphatase), is a member of the PTP family signaling proteins. Phosphotyrosine-based signaling of this non-transmembrane protein is essential for regulating cell growth, development, differentiation, survival, and migration. In particular, PTPN2 received researchers' attention when Manguso et al.

TIFA promotes colorectal cancer cell proliferation in an RSK- and PRAS40-dependent manner.

Previous studies have reported that TIFA plays different roles in various tumor types. However, the function of TIFA in colorectal cancer (CRC) remains unclear. Here, we showed that the expression of TIFA was markedly increased in CRC versus normal tissue, and positively correlated with CRC TNM stages.

PFKFB4 promotes angiogenesis via IL-6/STAT5A/P-STAT5 signaling in breast cancer.

Breast cancer has become the most newly-diagnosed cancer and the 5 leading cause of cancer death worldwide. The 5-year survival rate of breast cancer is about 90%. However, the 5-year survival rate drops to <30% when metastasis to distant sites occurs.

MCP-1 targeting: Shutting off an engine for tumor development.

A large amount of research has proven that monocyte chemotactic protein-1 (MCP-1) is associated with different types of disease, including autoimmune, metabolic and cardiovascular diseases. In addition, several studies have found that MCP-1 is associated with tumor development. MCP-1 expression level in the tumor microenvironment is associated with tumor development, including in tumor invasion and metastasis, angiogenesis, and immune cell infiltration.

Erratum: CCL16 maintains stem cell-like properties in breast cancer by activating CCR2/GSK3β/β-catenin/OCT4 axis: Erratum.

[This corrects the article DOI: 10.7150/thno.51000.

CCL16 maintains stem cell-like properties in breast cancer by activating CCR2/GSK3β/β-catenin/OCT4 axis.

Considerable evidence suggests that breast cancer metastasis and recurrence occur due to emergence of cancer stem cells (CSCs). In our previous study, we designed a high-throughput siRNA screening platform that identifies inflammation genes involved in the regulation of cancer cell stemness. We reported that CCL16 protein decreases OCT4 expression and reduces the ALDH+ subpopulation.