克服失巢凋亡是肿瘤转移和侵袭过程中所必需的。最近，据报道失巢凋亡参与肿瘤免疫并已被用于构建预后预测模型。然而，失巢凋亡在调节乳腺癌肿瘤免疫和药物敏感性中的作用仍不清楚，因此值得揭示。TCGA和GEO数据是基因表达谱的来源，用于识别失巢凋亡相关基因（ARG）基于子类型。 R4.2用于数据分析。乳腺癌分为三个亚组，其中在泛癌队列中表现出预后差异，ACC、BLCA、BRCA、LUAD、MESO、PAAD和SKCM。在乳腺癌中，其临床特征、免疫细胞浸润和药物敏感性表现出显着差异。机器学习构建预后预测模型，有助于进行化疗敏感性分层。随后，TJP3 被鉴定并验证为关键 ARG，其上调可增加紫杉醇诱导的细胞毒性的耐受性，同时伴随 caspas3 和 cleaved-caspase3 表达的增加。此外，TJP3的下调减弱了细胞迁移，伴随着E-cad表达增加和vimentin、twist1、zeb1和MMP7表达减少。此外，PD-L1的表达水平与TJP3呈负相关。基于ARGs的亚组分层有助于识别化疗敏感队列，也有助于预测临床结果。 TJP3 促进乳腺癌的化疗耐药性、肿瘤转移和潜在的免疫治疗逃避。

Overcoming anoikis is a necessity during the metastasis and invasion of tumors. Recently, anoikis has been reported to be involved in tumor immunity and has been used to construct prognosis prediction models. However, the roles of anoikis in regulating tumor immunity and drug sensitivity in breast cancer are still not clear and therefore worth uncovering.TCGA and GEO data are the source of gene expression profiles, which are used to identify anoikis-related-gene (ARG)-based subtypes. R4.2 is used for data analysis.Breast cancer is divided into three subgroups, amongst which shows prognosis differences in pan-cancer cohort, ACC, BLCA, BRCA, LUAD, MESO, PAAD, and SKCM. In breast cancer, it shows significant differences in clinical features, immune cell infiltration and drug sensitivity. Machine learning constructs prognosis prediction model, which is useful to perform chemotherapy sensitivity stratification. Following, TJP3 is identified and verified as the key ARG, up-regulation of which increases tolerance of paclitaxel-induced cell toxicity, accompanied with increased expression of caspas3 and cleaved-caspase3. In addition, Down-regulation of TJP3 weakens the cell migration, which accompanied with increased expression of E-cad and decreased expression of vimentin, twist1, zeb1, and MMP7. Furthermore, the expression level of PD-L1 is negative correlated with TJP3.ARGs-based subgroup stratification is useful to recognize chemotherapy sensitive cohort, and also is useful to predict clinical outcome. TJP3 promotes chemoresistance, tumor metastasis and potential immunotherapy escape in breast cancer.