FUNCTIONS OF APOLIPOPROTEINS IN CANCER APOPTOSIS

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 我们继续研究载脂蛋白L1（ApoL 1）和ApoL 2在诱导自噬（一种自食机制）中的功能，以及癌细胞死亡。细胞通常利用自噬来回收诸如氨基酸、核酸和脂肪酸的构件，以再合成大分子，诸如蛋白质、DNA和RNA以及脂质。最近的研究还表明，自噬可以作为一种程序性细胞死亡机制来清除受损细胞。我们最近的研究结果表明，ApoL 1是诱导各种癌细胞自噬性细胞死亡的分子调节因子之一，其密切相关的蛋白ApoL 2可以协同增强ApoL 1诱导的细胞死亡。ApoL 1和L2是人类癌症诊断、预后和治疗的潜在生物标志物。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. We continue investigating functions of apolipoprotein L1 (ApoL1) and ApoL2 in the induction of autophagy, a self-eating mechanism, in cancer cell death. Autophagy is normally used by cells to recycle the building blocks, such as amino acids, nucleic acids and fatty acids, for resynthesize macromolecules, such as proteins, DNA and RNA and lipids. Recent study also showed that autophagy can function as a programmed cell death mechanism to eliminate damaged cells. Our recent results showed that ApoL1 is one of the molecular regulators that induces autophagic cell death in various cancer cell types and its closely related protein ApoL2 can synergistically enhance ApoL1-induced cell death. Both ApoL1 and L2 are potential biomarkers for diagnosis, prognosis and treatment of human cancers.