Breast cancer is the most commonly diagnosed malignancy in women worldwide.Recently, uncontrolled expression of microRNAs was detected in several human disorders like cardiovascular, neurological, intestinal and autoimmunity diseases. MicroRNAs (miRNAs) are now investigated as novel prognostic and diagnostic biomarkers for several solid tumors like breast, lung, and gastrointestinal cancers. Current data suggest that miRNAs are implicated in various oncogenic processes implicated in breast cancer carcinogenesis trough modulating canonical Wnt pathway. Aberrant activation of Wnt/b-catenin signaling was shown to be significantly associated with tumor progression and poor prognosis in patients with breast cancer.This review presents recent findings on the molecular mechanism of microRNAs in regulation of Wnt/β-catenin signaling involved in tumorigenesis of breast cancer.

Context: Tachykinins (TKs), an evolutionarily conserved family of peptide hormones, are widely distributed within the peripheral and central nervous systems. TKs exert their biological actions in many processes via three subtypes of transmembrane G-protein coupled receptors, which are NK1R, NK2R, and NK3R. Although the mechanisms that connect TKs peptide activity to physiological processes are currently precise, it has been shown that TKs over-activation is associated with the pathogenesis of many diseases, including pain, emesis, depression, stress, and inflammatory processes, as well as human tumors. Gastrointestinal (GI) cancers refer to malignant conditions of the GI tract, which are among the most prevalent diseases and are the leading cause of cancerrelated death worldwide. Recent studies have shown that the binding of TKs to specific cellular receptors mediates a critical GI tumor proliferation pathway via initiation and activation of effector mechanisms, including protein synthesis and progression of the eukaryotic cell cycle. Evidence Acquisition: This study reviewed the role of tachykinins in the initiation and progression of gastrointestinal cancers. In this regard we searched databases such as PubMed, Science Direct, Google Scholar, and Scopus databases by using these keywords "Tachykinins", "Gastrointestinal cancer", "Metastasis", "G-protein coupled receptors", and "pharmacological inhibitor" without any time limit. The relevance of studies was identified by reviewing the titles and the abstracts. A total of 100 English language articles including experimental, observational, molecular, and cellular studies were reviewed. Results: The administration of the gastrointestinal cancer cells with Tk receptor antagonists induces apoptotic cell death through the tachykinin-mediated pathway. The findings showed that the pharmacological inhibition of TKRs with its selective antagonists has a promising prospect for the GI cancers treatment approach, either as a single agent or in combination with other chemotherapeutic agents. Conclusions: In this review, we presented different facts regarding the role of TKs and TKRs in the pathogenesis of GI malignancies for a better understanding and hence better management of these cancers. Therefore, understanding the underlying mechanism of the TK/TKR system can help to have a more excellent clinical vision for the treatment of GI cancers.

The immune system's role in maintaining the health of the gastrointestinal (GI) system is like a double-edged sword. Simultaneously, it could reduce the risk of pathogen invasion by the inflammatory response. But, if regulated improperly, it could also propagate oncogenic signaling that transfers a normal cell into the malignant counterpart. Thus far, several mechanisms have been proposed, such as the immune system could disturb the GI homeostasis and increase the survival and proliferative capacity of cells leading to the formation of a wide range of malignancies. Among the endless list of these mechanisms, inflammatory responses are currently fascinating research areas, as this response regulation is with the gut microbiota. Given this, the manipulation of microbiota might be a convenient and efficient way to prevent GI cancers. Probiotics could potentially achieve this by overturning the milieu in favor of normal gut homeostasis. In addition to the safety of use of probiotics, along with their potential ability to interact with immune system responses, led these bacteria to be viewed differently from dietary supplements. In the present review, we aimed to look into the mechanisms through which probiotics modulate the immune responses to stimulate anti-inflammatory responses and promote immune surveillance against neoplastic cells.