Bisdemethoxycurcumin (BDMC) is a demethoxy derivative of curcumin. In this study, a human gastric adenocarcinoma xenograft model was generated in vivo using nude mice and BDMC was observed to suppress the growth and activity of tumors, in addition to improving the physical and mental capacity of the mice. An increased number of apoptotic cells, decreased ratio of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein and increased caspase-3 expression was also observed following treatment with BDMC, indicating that BDMC may promote apoptosis in tumors via mitochondrial modulation. The growth of SGC 7901 gastric cancer cells was inhibited and arrested at G1 phase. Specific indicators of mitochondrial dysfunction, a reduction in adenosine triphosphate generation, the inner mitochondrial membrane potential, augmentation of reactive oxygen species production and cytochrome c were also detected in the mitochondria following treatment with BDMC. These results indicate that BDMC attenuates gastric adenocarcinoma growth by inducing mitochondrial dysfunction.

The study is aimed at exploring the potential biological process and molecular mechanism of KIF22 involved in the development and progression of pancreatic cancer. First, we used the GEPIA database and tissue qRT-PCR to examine the expression of KIF22 mRNA in pancreatic cancer. Meanwhile, immunohistochemistry revealed the presence of KIF22 in 71 pancreatic cancer tissues versus 30 paracarcinoma tissues. Then, we also explored the relationship between KIF22 expression level and clinical prognosis. Furthermore, in pancreatic cancer cells, we silenced KIF22 by transfecting KIF22 SiRNA, and we investigated the effect of KIF22 on the proliferation of pancreatic cancer cells with MTT and colony formation assays. Finally, we used Gene Set Enrichment Analysis (GSEA) to look at the effect of KIF22 on the cell cycle regulation of pancreatic cancer cells, and we used Western blot to look at the relationship between KIF22 and the phosphorylated MEK1/2, ERK1/2 (p-MEK1/2, p-ERK1/2), and the cyclin-dependent kinase inhibitor (P21). In this study, we found that KIF22 was highly expressed in pancreatic cancer tissues, and patients with high expression of KIF22 demonstrated significantly worse clinical prognosis outcomes ( P < 0.05 ). When the KIF22 gene was silenced in pancreatic cancer cells (PANC-1 and MIA PaCa-2), the cells’ ability to proliferate was significantly reduced. Furthermore, GSEA confirmed that KIF22 is involved in cell cycle regulation in pancreatic cancer patients ( FDR = 0.00158 , P < 0.0001 ). Besides, the level of KIF22 expression was positively correlated with Ki67 ( r = 0.8043 , P < 0.0001 ), and KIF22 can promote the transmutation of G1/S. The expression of p-MEK1/2 and p-ERK1/2 was significantly downregulated, while P21 expression was significantly upregulated ( P < 0.05 ). According to our findings, KIF22 is highly expressed in pancreatic cancer and demonstrates a poor clinical prognosis. It regulates the cell cycle via the MEK/ERK/P21 signaling axis and promotes the development of pancreatic cancer.