SEC23, the core component of the coat protein complex II (COPII), functions to transport newly synthesized proteins and lipids from the endoplasmic reticulum (ER) to the Golgi apparatus in cells for secretion. SEC23 protein has two isoforms (SEC23A and SEC23B) and their aberrant expression and mutations were reported to cause human diseases and oncogenesis, whereas SEC23A and SEC23B may have the opposite activity in human cancer, for a reason that remains unclear. This review summarizes recent research in SEC23, COPII-vesicle transportation, autophagy, and cancer.

Bladder cancer is the most common malignancy of the urinary tract, and ~50% of patients with bladder cancer experience recurrence and metastasis. The results of mass spectrometry revealed that the expression of zinc finger and BTB domain-containing 38 (ZBTB38) was higher in highly aggressive human bladder cancer 253J B-V cells compared with in the less aggressive bladder cancer 253J cells. However, the association between ZBTB38 and bladder cancer is currently not well defined, and the association of ZBTB38 with migration and invasive growth of bladder cancer cells remains unclear. Previous studies have suggested that ZBTB38 may act as an oncogene, similar to Kaiso. Furthermore, analysis of a clinical database suggested that ZBTB38 expression may be associated with poor prognosis of patients with bladder cancer. Using cell proliferation, migration and invasion assays, and western blotting, the present study demonstrated that ZBTB38 promoted the migration and invasive growth of bladder cancer cells, but inhibited their proliferation. Further experiments suggested that ZBTB38 promoted epithelial-mesenchymal transition and the expression levels of genes downstream of the Wnt/β-catenin signaling pathway. Notably, further experiments using a xenograft tumor metastasis model revealed that ZBTB38 promoted bladder cancer lung metastasis in vivo. These findings suggested that ZBTB38 promoted migration and invasive growth of bladder cancer cells through facilitation of the Wnt/β-catenin signaling pathway. To the best of our knowledge, this is the first study to reveal that ZBTB38 may promote migration and invasive growth of bladder cancer cells via modulation of the Wnt/β-catenin signaling pathway.

Background: Since metastasis is the primary cause of death in human colorectal cancer (CRC) patients, the exact mechanism underlying CRC metastasis remains unclear. Here, we provide evidence for a unique function of HomeoboxC10 (HOXC10) in driving CRC metastasis, as well as treatment options for these subpopulation patients. Methods: Immunohistochemistry detected the expression of HOXC10 in the human CRC cohort. The function of HOXC10 in CRC metastasis was investigated using the cecum orthotopic model. Results: In CRC patients, elevated expression of HOXC10 expression was linked to lymph node metastases, distant metastasis, worse tumor differentiation, higher AJCC stage, and poor prognosis. HOXC10 is also an independent predictive predictor for CRC patients (P<0.001). HOXC10 overexpression increased the metastasis ability of MC38 cells and promoted the infiltration of MDSCs by upregulating CXCL5 at the same time. The CXCR2 inhibitor can reduce the rate of metastasis in MC38 cells by reducing MDSCs infiltration. SB225002, a CXCR2 inhibitor, and anti-programmed death-ligand 1 (anti-PD-L1) can significantly prevent CRC metastasis. Conclusions: HOXC10 overexpression upregulated CXCL5, which promoted MDSCs infiltration. Interrupting this loop might be a potential therapy option for HOXC10-induced CRC metastasis.