KB-1471A8.2（简称KB）是我们通过lncRNA芯片筛选获得的、低表达于耐药卵巢癌组织、功能未知的一条lncRNA。前期发现，多种卵巢癌耐药细胞株中KB普遍低表达；过表达KB可显著逆转肿瘤细胞的耐药性；生物信息学分析及实验验证DEPTOR可能是KB调控的下游靶标，而文献已报道DEPTOR可通过抑制mTOR、诱导自噬的机制改变肿瘤细胞耐药；我们则发现过表达KB也可降低卵巢癌耐药细胞的自噬水平。因此，我们提出KB靶向调节DEPTOR、调控自噬、影响卵巢癌细胞耐药的新机制。研究拟阐明KB的生物学特征；以过表达/表达沉默技术，体内、体外评估KB在卵巢癌耐药中的作用；以DEPTOR为线索，采用挽救策略，论证其通过自噬调控卵巢癌耐药的分子机制。目前未见该lncRNA相关研究报道，本研究有望为逆转卵巢癌耐药提供新靶标。

KB-1471A8.2, a lncRNA of unknown function, was screened from lncRNA microarray and specially low-expressed in chemotherapy-resistant ovarian tumor tissue. Our previous study indicated that KB-1471A8.2 was down-regulated in a number of drug-resistant ovarian cancer cell lines and over-expression of KB-1471A8.2 in resistant cell lines could significant increase cells sensitive to anti-tumor drug. Bioinformatic analysis and experiment data indicated that DEPTOR, an specific inhibited protein of mTOR, could be a candidate target gene of KB-1471A8.2. Literature reported that DEPTOR could regulate drug resistance in some types of cancer through inhibiting mTOR then inducing autophagy, and we verified that the level of autophagy in chemotherapy-resistant ovarian cancer cell lines declined when KB-1471A8.2 was over-expressed. Base on these data, we propose a scientific hypothesis that KB-1471A8.2 regulated chemoresistance in ovarian cancer by DEPTOR modulating autophagy of cancer cell. Using DEPTOR as a mechanism clue, we will further investigate biological characteristics and regulatory mechanism of KB-1471A8.2 in ovarian cancer. Up to now, there is no report of KB-1471A8.2 in chemoresistance of ovarian cancer. This study may provide a therapeutics target of ovarian carcinoma.