Molecular & Cellular Toxicology ( IF 1.7 ) Pub Date : 2023-08-29 , DOI: 10.1007/s13273-023-00382-x Xinyu Gao , Yongfang Jiang
Background
Multiple myeloma (MM) is a common type of hematological malignancy. Cell adhesion molecule L1 (CHL1) can regulate the progression of a variety of tumors. However, the role of CHL1 is rarely reported in MM and the underlying mechanism is unclear.
Objective
The aim of this study is to uncover the possible effects of CHL1 on the autophagy and apoptosis of multiple myeloma (MM) cells and uncover the mechanism.
Results
We found the expression of CHL1 in MM patients was lower than that in healthy volunteers. CHL1 inhibited MM cell growth. In addition, CHL1 contributed to the apoptosis and autophagy of MM cells. Mechanically, we found CHL1 promoted autophagy and apoptosis of MM cells through regulating Hedgehog pathway.
Conclusion
We therefore thought CHL1may be a potential target for treating MM.
中文翻译:
CHL1通过抑制Hedgehog通路促进多发性骨髓瘤细胞自噬和凋亡
背景
多发性骨髓瘤(MM)是一种常见的血液恶性肿瘤。细胞粘附分子L1(CHL1)可以调节多种肿瘤的进展。然而,CHL1在MM中的作用鲜有报道,其潜在机制尚不清楚。
客观的
本研究的目的是揭示CHL1对多发性骨髓瘤(MM)细胞自噬和凋亡的可能影响并揭示其机制。
结果
我们发现MM患者中CHL1的表达低于健康志愿者。CHL1 抑制 MM 细胞生长。此外,CHL1有助于MM细胞的凋亡和自噬。从机制上讲,我们发现CHL1通过调节Hedgehog通路促进MM细胞的自噬和凋亡。
结论
因此我们认为 CHL1 可能是治疗 MM 的潜在靶点。