Long non-coding RNAs (lncRNAs) are a class of non-coding RNAs that play an essential role in various cellular activities, such as differentiation, proliferation, and apoptosis. Dysregulation of lncRNAs serves a fundamental role in the progression and initiation of various diseases, including cancer. Precision medicine is a suitable and optimal treatment method for cancer so that based on each patient’s genetic content, a specific treatment or drug is prescribed. The rapid advancement of science and technology in recent years has led to many successes in this particular treatment. Phytochemicals are a group of natural compounds extracted from fruits, vegetables, and plants. Through the downregulation of oncogenic lncRNAs or upregulation of tumor suppressor lncRNAs, these bioactive compounds can inhibit metastasis, proliferation, invasion, migration, and cancer cells. These natural products can be a novel and alternative strategy for cancer treatment and improve tumor cells’ sensitivity to standard adjuvant therapies. This review will discuss the antineoplastic effects of bioactive plant secondary metabolites (phytochemicals) via regulation of expression of lncRNAs in various human cancers and their potential for the treatment and prevention of human cancers.

Cancer immunotherapy is a promising approach for treating malignancies through the activation of anti-tumor immunity. However, the effectiveness and safety of immunotherapy can be limited by tumor complexity and heterogeneity, caused by the diverse molecular and cellular features of tumors and their microenvironments. Undifferentiated tumor cell niches, which we refer to as the “Origin of Tumor Development” (OTD) cellular population, are believed to be the source of these variations and cellular heterogeneity. From our perspective, the existence of distinct features within the OTD is expected to play a significant role in shaping the unique tumor characteristics observed in each patient. Single-cell transcriptomics is a high-resolution and high-throughput technique that provides insights into the genetic signatures of individual tumor cells, revealing mechanisms of tumor development, progression, and immune evasion. In this review, we explain how single-cell transcriptomics can be used to develop personalized cancer immunotherapy by identifying potential biomarkers and targets specific to each patient, such as immune checkpoint and tumor-infiltrating lymphocyte function, for targeting the OTD. Furthermore, in addition to offering a possible workflow, we discuss the future directions of, and perspectives on, single-cell transcriptomics, such as the development of powerful analytical tools and databases, that will aid in unlocking personalized cancer immunotherapy through the targeting of the patient’s cellular OTD.

Background The process of breast tumor dedifferentiation is complex and unclear. The mechanism represents the origin of the genesis and development of high-grade breast stem cells. It seems that microRNAs have crucial regulatory functions in this complicated phenomenon. The main objective of this study is to identify a potential "breast tumor stemness miRNA cluster" using an in silico strategy and qRT-PCR validation guided by the molecular pattern of mammary gland development (MGD). Methods Microarray databases GEO and ArrayExpress were used to determine mRNA and microRNA expression in different grades of breast carcinoma (BC). Differential gene expression of mRNA (GSE29044) and miRNA (GSE4566) in three grades of BC was analyzed using GEO2R compared with normal tissue. The enrichment results revealed MGD -associated mechanisms and target mRNAs. Using the BC database, the interaction between target mRNAs and significantly altered miRNAs (PV ≤ 0.05) in each BC grade was found by miRNet. After confirming our results using the GSE26659 data, the expression of the target miRNAs in tissue samples (24 BC, 17 normal tissues) was examined by real-time PCR. miRwalk and the STRING database discovered the miRNAs of interest and mRNA networks. Results The MGD stages of puberty, pregnancy and lactation, and mammary gland epithelial development were significantly involved in the upregulated genes of GI and GII tumors. No significant upregulated MGD mechanisms were detected in GIII BC. In silico analysis revealed that miRs 7/17/155 had an upregulation pattern and miR-26a had a downregulation pattern. qPCR showed that the miRNAs 7/17/155 were significantly upregulated in GIII tumors (PV ≤ 0.05), while there were no notable changes in miR-26a. EGFR was the central node regulated by the miR 7/17/155 intermediate mRNA cluster. Conclusions Our results suggest that microRNAs 7/17/155 may be a potential cluster associated with formation of breast tumor stemness. This cluster can be used for the breast cancer dedifferentiation therapy or molecular classification of mammary tumor differentiation status.