Breast cancer is the most prevalent malignant tumor and a leading cause of mortality among females worldwide. The tumorigenesis and progression of breast cancer involve complex pathophysiological processes, which may be mediated by post-translational modifications (PTMs) of proteins, stimulated by various genes and signaling pathways. Studies into PTMs have long been dominated by the investigation of protein phosphorylation and histone epigenetic modifications. However, with great advances in proteomic techniques, several other PTMs, such as acetylation, glycosylation, sumoylation, methylation, ubiquitination, citrullination, and palmitoylation have been confirmed in breast cancer. Nevertheless, the mechanisms, effects, and inhibitors of these unconventional PTMs (particularly, the non-histone modifications other than phosphorylation) received comparatively little attention. Therefore, in this review, we illustrate the functions of these PTMs and highlight their impact on the oncogenesis and progression of breast cancer. Identification of novel potential therapeutic drugs targeting PTMs and development of biological markers for the detection of breast cancer would be significantly valuable for the efficient selection of therapeutic regimens and prediction of disease prognosis in patients with breast cancer.

Background: Long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) plays a positive role in the progression of human malignant tumors. However, the molecular mechanism of SNHG1 remains elusive in breast cancer. Results: LncRNA SNHG1 was upregulated and had a positive relationship with poor prognosis according to bioinformatics analysis in pan-cancer including breast cancer. Silencing SNHG1 inhibited tumorigenesis in breast cancer both in vitro and in vivo. Mechanistically, SNHG1 functioned as a competing endogenous RNA (ceRNA) to promote TERT expression by sponging miR-18b-5p in breast cancer. miR-18b-5p acted as a tumor repressor in breast cancer. Moreover, the combination of SNHG1 knockdown and TERT inhibitor administration showed a synergistic inhibitory effect on breast cancer growth in vivo. Finally, E2F1 as a transcription factor, binding to SNHG1 promoter and enhanced SNHG1 transcription in breast cancer. Conclusions: Our results provide a comprehensive understanding of the oncogenic mechanism of lncRNA SNHG1 in breast cancer. Importantly, we identified a novel E2F1–SNHG1–miR-18b-5p–TERT axis, which may be a potential therapeutic target for breast cancer. Our results also provided a potential treatment for breast cancer when knockdown SNHG1 and TERT inhibitor administration simultaneously.

Breast cancer (BC) leads to the most amounts of deaths among women. Chemo-, endocrine-, and targeted therapies are the mainstay drug treatments for BC in the clinic. However, drug resistance is a major obstacle for BC patients, and it leads to poor prognosis. Accumulating evidences suggested that noncoding RNAs (ncRNAs) are intricately linked to a wide range of pathological processes, including drug resistance. Till date, the correlation between drug resistance and ncRNAs is not completely understood in BC. Herein, we comprehensively summarized a dysregulated ncRNAs landscape that promotes or inhibits drug resistance in chemo-, endocrine-, and targeted BC therapies. Our review will pave way for the effective management of drug resistance by targeting oncogenic ncRNAs, which, in turn will promote drug sensitivity of BC in the future.

Triple negative breast cancer (TNBC) is characterized as an estrogen receptor (ER) negative, progesterone receptor (PR) negative, and human epidermal growth factor receptor (HER-2) negative disease with an enhanced systemic metastatic incidence, chemotherapeutic insensitivity, and drug resistance. The internal characteristics of TNBC are extraordinary complex and are accompanied by numerous gene mutations and constitutively activated signaling networks, which, in turn, augment TNBC malignancy. There is an urgency to uncover new and potent therapeutic targets for TNBC. Herein, we discussed the historical as well as newly discovered subtypes and properties of TNBC. We also presented a systematic outline of the aberrant gene expression and abnormal activated signaling networks in TNBC. Subsequently, we summarized the corresponding targeted therapeutic drugs, and reviewed the current targeted TNBC therapies launched in clinical trials, thereby providing a direction for future TNBC therapy. We also provided a detailed list of coding genes involved in chemo-sensitive and chemo-resistance of TNBC, which can potentially serve as indicators of chemotherapeutic efficacy. Finally, we discussed the novel and future potential treatments of TNBC. This review highlighted the new era of TNBC treatment in the coming years and provided the gene expression profile of TNBC patients who may benefit from chemotherapy.

Breast cancer (BC) is the most common cause of deaths. Although recent medical advancements have improved survival of BC patients, the occurrence of metastasis increases mortality rate. Noncoding RNAs (ncRNAs) play important roles in BC metastasis (BCM). However, a detailed summary of ncRNAs involved in BCM is unavailable. Therefore, this review summarizes the key biological steps involved in BCM. We discussed the ncRNAs related to BCM according to “seed and soil” theory from four perspectives: (i) ncRNAs that make “breast cancer seed” preferable for BCM; (ii) ncRNAs that make “breast cancer seed” difficult for BCM; (iii) ncRNAs that make “breast cancer soil” preferable for BCM; (iv) ncRNAs that make “breast cancer soil” difficult for BCM. Lastly, we listed the ncRNAs and coding genes involved in BCM that act as initiators or suppressors. This review comprehensively overviews the biological mechanisms underlying BCM. The compiled evidence highlights the role of BCM-associated ncRNAs, which may serve as promising therapeutic targets for BCM.