During mammalian spermatogenesis, primordial germ cells develop into spermatogonia, giving rise to spermatocytes that undergo two meiotic divisions to become round spermatids. These cells differentiate into spermatozoa during spermiogenesis. Spermatogenesis is a complex process of cell differentiation controlled by many factors, among which gene regulation in the spermatogenic cells plays a pivotal role. Genes important for male gametogenesis involved in highly con-served landmark events such as meiotic recombination, formation of the synaptonemal complex, sister chromatid cohesion, spermiogenesis during postmeiotic stages, and checkpoints and factors required for the meiotic cell cycle. Spermatogenesis is characterized by phase-specific expression of many genes exclusively expressed in the spermatogenic cells. With the development and application of technologies like gene cloning, gene expression and functional characterization, many spermatogenesis-related genes have been found in the past few years, and some of them have been proved to play an important role in spermatogenesis. Here, we review the advances in this field with an emphasis on spermatogenesis-associated genes such as cyclins, proto-oncogenes, azoospermia factor genes, cytoskeleton genes, heat shock genes, nucleoprotein transition genes, centrin genes and apoptosis genes.
Spermatogenesis is a highly regulated developmental process. During spermatogenesis, the replacement of histones by protamine plays an important role in repackaging the haploid genome of the sperm nuclear. The spermatozoan nucleus of the Decapoda is decondensed. Presently, many studies have proved that histones and histone modifications were retained in the nucleus or acrosome structure of the Decapoda spermatozoa. This review summarizes the dynamic characteristics of histones during spermatogenesis in Decapoda and helps clarify the mechanism of the decondensed chromatin structure.
TMEM16A plays a vital role in various physiological activities in the human body, and it is a potential drug target for many diseases. Recently, several studies have shown that the high expression of TMEM16A in lung cancer is closely related to the proliferation and migration of lung cancer cells. This work demonstrates that crocin is a new natural-product inhibitor of TMEM16A and it can inhibit the proliferation and migration of lung cancer cells through TMEM16A. Our results showed that crocin inhibits TMEM16A whole-cell currents in a concentration-dependent manner with an IC 50 value of 38.32 ± 2.31 μM. CCK8 and wound healing studies showed that crocin inhibits the proliferation and migration of lung cancer cells LA795 and NCI-H1299 in a concentration-dependent manner; however, it does not affect the proliferation and migration of 2BS cells. In addition, the inhibitory effect of crocin on the proliferation and migration of LA795 cells can be overcome by knockdown of TMEM16A using shRNA. In conclusion, this work suggests that TMEM16A is a potential drug target of crocin as it can inhibit the proliferation and migration of lung cancer. Crocin can be further evaluated as an intriguing lead for lung cancer treatment.
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