Baicalein, an active ingredient separated from Astragalus membranaceus, has shown its anticancer ability in various cancers. However, its effect on nasopharyngeal carcinoma has not been explored yet. The present study aimed to investigate the effect of baicalein on the growth, proliferation, apoptosis, and cell cycle of human nasopharyngeal carcinoma cells, as well as transplanted nude mouse xenograft. The results showed that baicalein inhibited the growth and proliferation of CNE1 and CNE2 cells in a time- and concentration-dependent manner. It also caused a significant increase in the number of cells in the G0/G1 phase and a decrease in the G2/M phase, thereby reducing the number of cells entering mitosis and inhibiting the proliferation of tumor cells. Baicalein also significantly induced apoptosis of CNE1 and CNE2 cells. Western blots showed that baicalein decreased the expression of Bcl-xl and Mcl-1 and increased the expression of Bax, Bad, and caspase 3, 8, and 9. In CNE1- and CNE2-transplanted tumors of mice, baicalein significantly inhibited tumor growth. In conclusion, baicalein could inhibit the growth and proliferation of human nasopharyngeal carcinoma cells, change their cell cycle, and induce apoptosis. Baicalein also effectively limits both CNE1- and CNE2-transplanted tumors in nude mice. Downregulation of Bcl-xl and Mcl-1 proteins and upregulation of Bax and Bad may be involved in the mechanism.

Lumbar intervertebral disc degeneration (IVDD) is the most common cause of low back pain (LBP). Among all the factors leading to IVDD, lumbar cartilage endplate (LCE) degeneration is considered a key factor. In the present study, we investigate the effect and regulation of carbonic anhydrase 12 (CA12) in LCE, which catalyzes hydration of CO 2 and participates in a variety of biological processes, including acid–base balance and calcification. Our results show that CA12, downregulated in degenerated LCE, could maintain anabolism and prevent calcification in the endplate. Furthermore, CA12 is regulated by the IGF-1/IGF-1R/PI3K/CREB signaling pathway. When we overexpressed CA12 in LCE, the decreased anabolism induced by inflammatory cytokine could be rescued. In contrast, reducing CA12 expression, either with siRNA, PI3Kinhibitor, or CREB inhibitor, could downregulate anabolism and cause apoptosis and then calcification in LCE. The protective effects of IGF-1 are even diminished with low-expressed CA12. Similar results are also obtained in an ex vivo model. Consequently, our results reveal a novel pathway, IGF-1/IGF-1R/PI3K/CREB/CA12, that takes a protective role in LCE degeneration by maintaining anabolism and preventing calcification and apoptosis. This study proposes a novel molecular target, CA12, to delay LCE degeneration.

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