Breast cancer is one of the most lethal malignancies in women in the world. Various factors are involved in the development and promotion of the malignancy; most of them involve changes in the expression of certain genes, such as microRNAs (miRNAs). MiRNAs can regulate signaling pathways negatively or positively, thereby affecting tumorigenesis and various aspects of cancer progression, particularly breast cancer. Besides, accumulating data demonstrated that miRNAs are a novel tool for prognosis and diagnosis of breast cancer patients. Herein, we will review the roles of these RNA molecules in several important signaling pathways, such as transforming growth factor, Wnt, Notch, nuclear factor‐κ B, phosphoinositide‐3‐kinase/Akt, and extracellular‐signal‐regulated kinase/mitogen activated protein kinase signaling pathways in breast cancer.

Background: Granulocyte colony-stimulating factor (G-CSF) expressed in engineered Escherichia coli (E. coli) as a recombinant protein is utilized as an adjunct to chemotherapy for improving neutropenia. Recombinant proteins overexpression may lead to creation of inclusion bodies whose recovery is a tedious and costly process. To overcome the problem of inclusion bodies, secretory production might be a used. To achieve a mature secretory protein product, suitable signal peptide (SP) selection is a vital step Objective: In the present study we aimed in silico evaluation of proper SPs for secretory production of recombinant G-CSF in E. coli Methods: Signal peptide website and UniProt were used to collect the SPs and G-CSF sequences. Then, SignalP were utilized in order to predict the SPs and location of their cleavage site. Physicochemical features and solubility were investigated by ProtParam and Protein-sol tools. Fusion proteins sub-cellular localization were predicted by ProtCompB Results: LPP, ELBP, TSH, HST3, ELBH, AIDA and PET were excluded according to SignalP. The highest aliphatic index belonged to OMPC, TORT and THIB and PPA. Also, the highest GRAVY belonged to OMPC, ELAP, TORT, BLAT, THIB, and PSPE. Furthermore, G-CSF fused with all SPs were predicted as soluble fusion proteins except three SPs. Finally, we found OMPT, OMPF, PHOE, LAMB, SAT, and OMPP can translocate G-CSF into extracellular space Conclusion: Six SPs were suitable for translocating G-CSF into the extracellular media. Although growing data indicated that the bioinformatics approaches can improve the precision and accuracy of studies, further experimental investigations are required for final validation

Breast cancer is a major clinical challenge that affects a wide range of the female population and heavily burdens the health system. In the past few decades, attempts have been made to understand the etiology of breast cancer, possible environmental risk factors, and the genetic predispositions, pathogenesis, and molecular aberrations involved in the process. Studies have shown that breast cancer is a heterogeneous entity; each subtype has its specific set of aberrations in different cell signaling pathways, such as Notch, Wnt/β‐catenin, transforming growth factor‐β, and mitogen‐activated protein kinase pathways. One novel group of molecules that have been shown to be inducted in the regulation of multiple cell signaling pathways is the long noncoding RNAs (lncRNAs). These molecules have important implications in the regulation of multiple signaling pathways by interacting with various genes, affecting the transcription process, and finally, playing roles in posttranslational control of these genes. There is growing evidence that lncRNAs are involved in the process of breast cancer formation by effecting the aforementioned signaling pathways, and that this involvement can have significant diagnostic and prognostic values in clinical contexts. The present review aims to elicit the significance of lncRNAs in the regulation of cell signaling pathways, and the resulting changes in cell survival, proliferation, and invasion, which are the hallmarks of breast cancer.

Statins, inhibitors of hydroxy methyl glutaryl coenzyme-A (HMG-CoA) reductase, are the most widely used drugs for treating hypercholesterolemia. However, statins can cause disabling myopathy as their main adverse effect. Several molecular mechanisms underlie the statin-induced myopathy including the decrease in the levels of essential mevalonate and cholesterol derivatives. This review discusses a further mechanism involving the loss of other anti-oxidant defenses besides ubiquinone (Co-Q) in skeletal muscles which produce a significant amount of reactive oxygen species (ROS). Therefore, to maintain their function, skeletal muscles need a high level of anti-oxidants.

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Background: Triple Negative breast cancer cases with no available targeted therapy and advanced cases of luminal and Her2+ that become resistant to available state-of-the-art treatments are priorities in cancer research. Immune checkpoint blockade, particularly PDL1/PD1 inhibition, is suggested as a potential option for these patients after achievement in several other types of cancers such as melanoma. However, the exact subpopulation of breast cancer patients that overexpress PDL1 is yet to be completely identified. Additionally, reports over the value of PDL1 as a biomarker for the prognosis of cancer and its correlation with clinicopathological features of malignancy are diverse. Method: In this study, we performed immunohistochemistry on 60 breast cancer – 22 triple negative and 38 Her2+ cases – and 20 paired lymph node samples. Results: PDL1 expression was present in 21.6% (13/60) of breast cancer samples. PDL1 expression is significantly associated with ER/PR negativity and the grade of the tumor. The association between PDL1 positivity and recurrence and the overall survival of patients was not significant. Conclusion: PDL1 expression is similar between triple-negative and non-luminal Her2+ cases, thus some of the advanced non-luminal Her2+ cases might be benefitted from immune checkpoint blockade.