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Background Adriamycin-based neoadjuvant chemotherapy is widely used in HER2- breast cancer patients, however, some patients have no response or acquire resistance to these regimens. Therefore, it is important to screen patients who respond to adriamycin with biomarkers. Methods A human lncRNA microarray analysis followed by a quantitative real-time polymerase chain reaction (qRT-PCR) assay was utilized to identify the differentially expressed lncRNAs. The proliferation viability of cells transfected with or without CTB 104H12.5 was measured by CCK-8 and clone formation assay, cell apoptosis and cell cycle were evaluated by Flow cytometry. And the expression of RNA and proteins was tested by qRT-PCR and Western blot, respectively. Results Ten whole blood samples from HER2- breast cancer patients who received docetaxel combined with adriamycin regimen were enrolled, a human lncRNA microarray analysis showed that the low expression of CTB-104H12.5 was associated unfavorable prognosis. And the mRNA and protein level of CTB-104H12.5 is much lower in MCF-7/ADR cells than that of MCF-7 cells while CTB-104H12.5 knockdown in MCF cells induces cell resistance to adriamycin, while CTB-104H12.5 overexpression in MCF7/ADR cells reversed their resistance to adriamycin. Also, the mRNA and protein levels of GAS7C were associated with CTB-104H12.5. Conclusions Low expression of CTB-10412.5 predicted resistance to adriamycin in HER2 negative breast cancer, which may serve as a potential biomarker to dynamically monitor adriamycin resistance for breast cancer patients.

Angiotensin II (AngII) is an important factor that promotes the proliferation of cancer cells, whereas celastrol exhibits a significant antitumor activity in various cancer models. Whether celastrol can effectively suppress AngII mediated cell proliferation remains unknown. In this study, we studied the effect of celastrol on AngII-induced HepG2 cell proliferation and evaluated its underlying mechanism. The results revealed that AngII was able to significantly promote HepG2 cell proliferation via up-regulating AngII type 1 (AT1) receptor expression, improving mitochondrial respiratory function, enhancing nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, increasing the levels of reactive oxygen species (ROS) and pro-inflammatory cytokines. The excess ROS from mitochondrial dysfunction is able to cause the apoptosis of tumor cells via activating caspase3 signal pathway. In addition, the reaction between NO and ROS results in the formation of peroxynitrite (ONOO-), and then promoting cell damage. celastrol dramatically enhanced ROS generation, thereby causing cell apoptosis through inhibiting mitochodrial respiratory function and boosting the expression levels of AngII type 2 (AT2) receptor without influencing NADPH oxidase activity. PD123319 as a special inhibitor of AT2R was able to effectively decreased the levels of inflammatory cytokines and endothelial nitric oxide synthase (eNOS) activity, but only partially attenuate the effect of celastrol on AnII mediated HepG2 cell proliferation. Thus, celastrol has the potential for use in liver cancer therapy. ROS derived from mitochondrial is an important factor for celastrol to suppress HepG2 cell proliferation.