Recent Advances in Comprehending the Signaling Pathways Involved in the Progression of Breast Cancer

Abstract

This review describes recent advances in the comprehension of signaling pathways involved in breast cancer progression. Calcium sensing receptor (CaSR), caveolae signaling, signaling referred to hypoxia-inducing factors and disturbances in the apoptotic machinery are related to more general biological mechanisms and are considered first. The others refer to signaling pathways of more specific biological mechanisms, namely the heparin/heparin-sulfate interactome, over-expression of miRNA-378a-5p, restriction of luminal and basal epithelial cells, fatty-acid synthesis, molecular pathways related to epithelial to mesenchimal transition (EMT), HER-2/neu gene amplification and protein expression, and the expression of other members of the epithelial growth factor receptor family. This progress in basic research is fundamental to foster the ongoing efforts that use the new genotyping technologies, and aim at defining new prognostic and predictive biomarkers for a better personalized management of breast cancer disease.

Breast Cancer Chemotherapeutic Options: A General Overview on the Preclinical Validation of a Multi-Target Ruthenium(III) Complex Lodged in Nucleolipid Nanosystems

“…Apoptosis unfolds through two different pathways: the intrinsic pathway-or mitochondria -activated by intracellular signals such as organelles or biomolecular damages (e.g., mitochondrial or DNA injury), and the extrinsic pathway-or death receptor-activated by extracellular signals, both propagated by caspase cascades ultimately leading to cell death [44]. Normally, escape of apoptosis in BCC takes place by definite mechanisms: perturbed signaling of death receptors, deficiency of caspase activity, as well as compromised balance between anti-apoptotic and pro-apoptotic proteins [45]. Bcl-2 protein family regulates the intrinsic pathway and consists of members that either promote (proapoptotic) or inhibit (antiapoptotic) programmed cell death by primarily controlling mitochondrial outer membrane permeabilization (MOMP).…”

“…In the context of cancer, genetic anomalies and unconventional microenvironments profit by endogenous pro-survival signaling to re-program and rewire metabolism to sustain survival, growth, and proliferation. It is now largely established that tumor is not simply a consequence of deregulated proliferation, but also of evasion from apoptosis, so the regulation of programmed cell death in cancer cells can be of critical importance in defining the overall growth or regression in response to treatments [45,47,152]. Besides being a major occurrence in the onset and progression of BC, malignant cells survival represents a crucial contributing factor also in clinical failure and chemoresistance development [153].…”

Copy number alterations associated with clinical features in an underrepresented population with breast cancer

“…Polymorphisms of single nucleotides or of larger DNA fragments and all the other abovementioned pathways are widely associated with the development of cancer in general. Aberrant activation of these pathways in breast cancer is part of the oncogenic mechanisms contributing to disease progression and is the focus of many current studies, since the disruption of mechanisms affected by these pathways may lead to pathogenic events (Mocellin, Valpione, Rossri, & Pooley, 2018;Nicolini, 2017.;Ziv et al, 2017). The description of these changes is very relevant from the point of view of genetic susceptibility.…”

Hypoxia: syndicating triple negative breast cancer against various therapeutic regimens

“…By this selective interaction, HIF-1α recruits JMJD2C to the hypoxia response elements of HIF-1 target genes, further reducing the histone H3 trimethylation at lysine 9, and enhancing HIF-1 binding to hypoxia response elements. The enhancement of HIF-1 binding to hypoxia response elements activates the transcription of PDK1, L1CAM, GLUT1, LOX, LOXL2, and LDHA mRNA in human BC biopsies ( 112 , 113 ). Lambert et al.…”