Breast cancer is a malignant tumor that has a high mortality rate and mostly occurs in women. Although significant progress has been made in the implementation of personalized treatment strategies for molecular subtypes in breast cancer, the therapeutic response is often not satisfactory. Studies have reported that long non-coding RNAs (lncRNAs) are abnormally expressed in breast cancer and closely related to the occurrence and development of breast cancer. In addition, the high tissue and cell-type specificity makes lncRNAs particularly attractive as diagnostic biomarkers, prognostic factors, and specific therapeutic targets. Therefore, an in-depth understanding of the regulatory mechanisms of lncRNAs in breast cancer is essential for developing new treatment strategies. In this review, we systematically elucidate the general characteristics, potential mechanisms, and targeted therapy of lncRNAs and discuss the emerging functions of lncRNAs in breast cancer. Additionally, we also highlight the advantages and challenges of using lncRNAs as biomarkers for diagnosis or therapeutic targets for drug resistance in breast cancer and present future perspectives in clinical practice.Long non-coding RNAs (lncRNAs) are originally thought to be the noise of transcripts in the genome and have no biological function. Recently, the function of lncRNAs is beginning to attract widespread attention. 7 Increasing studies have shown that lncRNAs are involved in various aspects of cellular physiological processes, such as proliferation, differentiation, migration, and apoptosis, by regulating gene transcription and post-transcriptional processing. 8,9 In addition, lncRNAs are closely related to the occurrence, development, and prognosis of various cancers, such as breast, liver, colon, and lung cancer and even leukemia. [10][11][12][13] According to lncRNA genomic position, subcellular localization, and function, they can be divided into six types (Figure 1). 14 (1) Enhancer lncRNAs are derived from the promoter enhancer region, such as lncRNA-LEENE. 15 (2) Intron lncRNAs are transcribed from the intron region of the gene. The gene-coding protein completely contained the intron lncRNA, which can stabilize the transcription or regulate the alternative splicing of the coding gene. (3) Antisense lncRNA: its transcription orientation is opposite to the transcription orientation of the adjacent protein-encoding gene, such as lncTALAM1 and PDCD4-AS1. 16,17 (4) The sense lncRNA: its transcription orientation is the same as that of the adjacent protein-encoding gene, such as lncRNAGAS5 and ecCEPBA. 18,19 (5) Intergenic lncRNA, which can be transcribed between two protein-coding genes, is an autonomously transcribed

Chronic stress results in disturbances of body hormones through the neuroendocrine system. Cancer patients often experience recurrent anxiety and restlessness during disease progression and treatment, which aggravates disease progression and hinders treatment effects. Recent studies have shown that chronic stress-regulated neuroendocrine systems secret hormones to activate many signaling pathways related to tumor development in tumor cells. The activated neuroendocrine system acts not only on tumor cells but also modulates the survival and metabolic changes of surrounding non-cancerous cells. Current clinical evidences also suggest that chronic stress affects the outcome of cancer treatment. However, in clinic, there is lack of effective treatment for chronic stress in cancer patients. In this review, we discuss the main mechanisms by which chronic stress regulates the tumor microenvironment, including functional regulation of tumor cells by stress hormones (stem cell-like properties, metastasis, angiogenesis, DNA damage accumulation, and apoptotic resistance), metabolic reprogramming and immune escape, and peritumor neuromodulation. Based on the current clinical treatment framework for cancer and chronic stress, we also summarize pharmacological and non-pharmacological therapeutic approaches to provide some directions for cancer therapy.

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