Y Fu

Background and Objectives Aconitine is a toxic substance capable of causing damage to the nervous system, digestive system, and gastric tissue. Wogonin exhibits significant antibacterial, antioxidant, and potential anticancer effects. The PI3K/Akt pathway is known to engage in the development of cancer cells. Consequently, it is of great significance to investigate the potential of wogonin on aconitine-induced gastric tissue damage in gastric cancer (GC) and its correlation with the signaling pathway. Materials and Methods Forty modelled mice were divided into a normal group, normal saline group, aconitine (low, high) dose group, wogonin (high, medium, low) dose group, celecoxib group, and Weifuchun group. After treatment, we detected the mouse’s tumor volume and survival day, as well as determined the expression of PI3K/Akt, LC3B, and p62. Results During modeling, HE staining revealed that the low-dose aconitine group exhibited improved pathological conditions, reduced tumor volume and mass compared to the saline group, and elevated survival days. After modeling, tumor volume and mass decreased concentration-dependent in each wogonin dose group. Wogonin treatment greatly prolongs survival days and effectively inhibits tumor growth. The expressions of LC3B, P62, PI3K, Akt, and mTOR mRNA were all decreased compared to the model group. Meanwhile, the treatment promoted the expression of LC3 and Beclin1 proteins related to the autophagy pathway. Conclusion Wogonin effectively ameliorates gastric tissue damage induced by aconitine in GC, prolongs the survival days of mice, and inhibits tumor growth through activation of the PI3K/Akt signaling pathway and reduction of P62 protein.

Tumor invasion and metastasis remain a major cause of mortality in breast cancer patients. It was reported that BP1, a homeobox isoform of DLX4, is overexpressed in 80% of breast cancer patients and in 100% of estrogen receptor negative (ER-) tumors. The prevalence of BP1 positive cells and the intensity of BP1 immunoreactivity increased with the extent of ductal proliferation and tumorigenesis. These findings imply that BP1 may play an important role in ER- breast cancer. I sought to determine the effects and mechanisms of BP1 on cell proliferation and metastasis using ER- Hs578T cells as a model. Cells were transfected with either pcDNA3.2 plasmid containing BP1 gene, or pcDNA3.2 vector, then selected and cloned. Overexpression of BP1 increased cell proliferation rate by 2-5 fold (p&#60;0.005), and enhanced the <i>in vitro </i>invasive activity by 25-65 fold (p&#60;0.001). Microarray experiments were performed to identify differentially expressed genes when BP1 is overexpressed. The gene expression profile of the transfected cell lines were compared, resulting in 71 differentially expressed genes with a fold-change of &#62;=2.0. Of those genes, 49 were up-regulated and 22 were down-regulated. Significant pathways were identified involving cell proliferation and metastasis. These data demonstrated that overexpression of BP1 significantly enhanced cell proliferation and metastatic potential in ER- Hs578T cells. Further analysis with more ER- cell lines and patient samples is warranted to establish BP1 as a therapeutic target.