3,3′,4,4′,5‐Polychlorinated biphenyl (PCB126) is a persistent organic environmental pollutant which can affect various biological activities of organisms, such as immunity, neurological function, and reproduction. In our study, we aimed to investigate the effects of PCB126 on granulosa cells (GCs). GCs were collected from ovaries in PMSG‐treated mice, after 24 hours culture. GCs were then incubated with 10 pg/mL, 100 pg/mL, and 10 ng/mL of PCB126 for another 24 hours. Following these steps, exposed GCs were collected for further experimentation. Our data showed that the number of GCs in the 10 ng/mL PCB126 decreased. Meanwhile, pyknotic nuclei and condensed chromatin increased, while the apoptotic cells in the 10 ng/mL PCB126 group were significantly increased. Furthermore, the expression of the apoptotic executive protein caspase‐3 increased after PCB126 treatment. The expression of Bax, Bcl‐2, and Bim related to the mitochondrial apoptosis pathway were also influenced to different degrees. Thus, our data suggested that PCB126 affect the GCs apoptosis, and mitochondrial apoptosis pathway was involved in this process.

Proper spindle orientation is essential for cell fate determination and tissue morphogenesis. Recently, accumulating studies have elucidated several factors that regulate spindle orientation, including geometric, internal and external cues. Abnormality in these factors generally leads to defects in the physiological functions of various organs and the development of severe diseases. Herein, we first review models that are commonly used for studying spindle orientation. We then review a conservative heterotrimeric complex critically involved in spindle orientation regulation in different models. Finally, we summarize some cues that affect spindle orientation and explore whether we can establish a model that precisely elucidates the effects of spindle orientation without interfusing other spindle functions. We aim to summarize current models used in spindle orientation studies and discuss whether we can build a model that disturbs spindle orientation alone. This can substantially improve our understanding of how spindle orientation is regulated and provide insights to investigate this complex event.

Radiotherapy (RT) resistance remains a substantial challenge in cancer therapy. Although physical factors are optimizing, the biological mechanisms for RT resistance are still elusive. Herein, we explored potential reasons for this difficult problem by generating RT-resistant models for in vitro and in vivo experiments. We found that abnormal spindle-like microcephaly-associated protein (ASPM) was highly expressed in RT-resistant samples and significantly correlated with disease advance in lung adenocarcinoma. Mechanistically, ASPM helps RT-resistant cells to evade spindle checkpoint surveillance and complete cell division after irradiation through destruction of microtubule stability, with subsequent increases in chromosome mis-segregation and deteriorating chromosomal stability during mitosis. Depletion of ASPM stabilized microtubules and significantly decreased chromosome mis-segregation, rendering RT-resistant cells renew sensitive to radiation. We further found, with bioinformatics analysis, amino acid sequence 963–1263 of ASPM as a potential new drug target for overcoming RT resistance and identified 9 drug pockets within this domain for clinical translation. Our findings suggest that ASPM is a key regulator with an important role in promoting RT resistance in non-small cell lung cancer, and that suppressing or blocking its expression could be worth exploring as therapy for a variety of RT-resistant cancers.