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Objective To screen out the immune-related LncRNA genes in triple-negative breast cancer (TNBC) and to construct a prognostic prediction model of TNBC. Methods ① We downloaded the transcriptome RNA expression profiling raw data of TNBC tissues and para-cancer tissues from the Cancer Genome Atlas (TCGA) project, and combined with the Immport database to screen TNBC immune-related lncRNAs. Furthermore, univariate and multivariate Cox analyses were used to screen immune-related lncRNAs closely related to TNBC and prognosis, and then immune-related ln cRNAs closely related to prognosis were determined according to the optimal AIC value. ② Based on the immune-related lncRNAs, the prognostic prediction model of TNBC was constructed. ③ The TNBC patient samples were divided into highrisk and low-risk groups based on the median of the risk score values calculated from the TNBC prognostic risk model, and survival was compared between the high- and low-risk groups. ④ ROC and principal component analysis (PCA） were used to evaluate the predictive efficacy of the TNBC prognostic prediction model. ⑤ Multivariate Cox analysis was used to analyze the independence of TNBC prognostic prediction model in predicting efficacy. Results A total of 369 immune-related lncRNAs were obtained from 65 TNBC tissue samples. Three immune-related lncRNAs (AC090181. 2, LINC01235, and LINC01943） were obtained by univariate and multivariate Cox analyses, and the prognostic prediction model of TNBC was constructed. The formula of the model was as follows： risk score (RS） = (– 6. 24904×AC090181. 2） + (0. 240562×LINC01235） + (–2. 18153×LINC01943). There was significant difference between the high-risk group and the low-risk group (P<0. 001). The predictive model of TNBC had a good predictive effect on the prognosis of patients (AUC = 0. 910； the distribution of projection points was different between the high- and low-risk groups, and the discrimination degree was high). TNBC prognostic prediction model could predict TNBC prognosis independently (HR=1. 028，P< 0. 05). Conclusion We have successfully constructed a prognostic prediction model consisting of three immune-related LncRNAs (AC090181. 2, LINC01235, and LINC01943） closely related to prognosis, which can better predict the prognosis of TNBC patients. [ABSTRACT FROM AUTHOR]

Objective To observe the effects of cyperenone combined with carboplatin on the proliferation and apoptosis of triple-negative breast cancer cell line MDA-MB-231, and to explore their mechanism. Methods MDA-MB-231 cells were divided into four groups: simple cell group, carboplatin-treated group, cyperenone-treated group, and cyperenone combined with carboplatin group. DMSO was added to the simple cell group, carboplatin (20 μmol/L) was added to the carboplatin group, cyperenone (0. 4 mmol/L) was added to the carboplatin-treated group, and carboplatin (20 μmol/L) and cyperenone (0. 4 mmol/L) were added to the carboplatin combined with carboplatin group. The cell survival rate of each group was measured by CCK-8 assay. The cell cloning ability of each group was observed by cell cloning experiment, which was expressed by cell colony number. The distribution of cell cycle and the rate of apoptosis were observed by flow cytometry. The endoplasmic reticulum stress-related proteins PERK, CHOP and apoptosis-related proteins BAX and Bcl-2 were detected by Western blotting. Results The cell survival rates of the carboplatin group and cyperenone group were lower than that of the simple cell group, while the cell survival rate of the cyperenone combined with carboplatin group was lower than those of the other three groups (all P<0. 05). The number of cell colonies in the simple cell group, carboplatin-treated group, cyperenone-treated group, and cyperenone combined with carboplatin group were 328 ± 18, 204 ± 10, 138 ± 13 and 47 ± 5, respectively, and there was significant difference between groups (all P<0. 05). The cell cycle of MDA-MB-231 was blocked in the G2/M phase in the carboplatin group, MDA-MB-231 cell cycle was blocked in the G0/G1 phase in the cyperenone group, and cell cycle of MDA-MB-231 was both blocked in the G2/M phase and G0/ G1 phase in the cyperenone combined with carboplatin group. The apoptosis rates of the carboplatin group and cyperenone group were higher than that of simple cell group, while the apoptosis rate of the cyperenone combined with carboplatin group was higher than those of the other three groups (all P<0. 05). Compared with the simple cell group, the relative expression levels of PERK, CHOP and Bax proteins significantly increased and the relative expression of Bcl-2 protein significantly decreased in the carboplatin group and cyperenone group (all P<0. 05). Compared with the other three groups, the relative expression levels of PERK, CHOP and Bax proteins significantly increased, and the relative expression of Bcl-2 protein significantly decreased in the cyperenone combined with carboplatin group (all P<0. 05). Conclusion The combination of cyperenone and carboplatin can inhibit the proliferation and promote the apoptosis of triple-negative breast cancer cells, and their mechanism may be related to the regulation of endoplasmic reticulum stress-mediated apoptosis pathway. [ABSTRACT FROM AUTHOR]