Our studies indicate that activation of RON signaling within breast cancer cells promotes tumor cell intrinsic growth and immune evasion which support breast cancer progression and highlight the role of targeting RON signaling as a potential therapeutic strategy against breast cancer.Pancreatic cancer is among the most detrimental tumors, with novel treatment options urgently needed. The pathological downregulation of a miRNA in tumors can lead to the overexpression of oncogenes, thus suggesting miRNA replacement as novel strategy in cancer therapy. While the role of miR24 in cancer, including pancreatic carcinoma, has been described as ambiguous, it may hold great promise and deserves further studies. Here, we comprehensively analyze the effects of miR24-3p replacement in a set of pancreatic carcinoma cell lines. Transfection of miR24-3p mimics leads to profound cell inhibition in various 2D and 3D cell assays, based on the induction of apoptosis, autophagy and ROS. Comprehensive analyses of miR24-3p effects on the molecular level reveal the transcriptional regulation of several important oncogenes and oncogenic pathways. Based on these findings, miRNA replacement therapy was preclinically explored by treating tumor xenograft-bearing mice with miR24-3p mimics formulated in polymeric nanoparticles. The obtained tumor inhibition was associated with the induction of apoptosis and necrosis. Taken together, we identify miR24-3p as powerful tumor-inhibitory miRNA for replacement therapy, and describe a complex network of oncogenic pathways affected by miR24.Primary cilia function as cells' antennas to detect and transduce external stimuli and play crucial roles in cell signaling and communication. https://www.selleckchem.com/products/Temsirolimus.html The vast majority of cilia genes that are causally linked with ciliopathies are also associated with neurological deficits, such as cognitive impairments. Yet, the roles of cilia dysfunctions in the pathogenesis of psychiatric disorders have not been studied. Our aim is to identify patterns of cilia gene dysregulation in the four major psychiatric disorders schizophrenia (SCZ), autism spectrum disorder (ASD), bipolar disorder (BP), and major depressive disorder (MDD). For this purpose, we acquired differentially expressed genes (DEGs) from the largest and most recent publicly available databases. We found that 42%, 24%, 17%, and 15% of brain-expressed cilia genes were significantly differentially expressed in SCZ, ASD, BP, and MDD, respectively. Several genes exhibited cross-disorder overlap, suggesting that typical cilia signaling pathways' dysfunctions determine susceptibility to more than one psychiatric disorder or may partially underlie their pathophysiology. Our study revealed that genes encoding proteins of almost all sub-cilia structural and functional compartments were dysregulated in the four psychiatric disorders. Strikingly, the genes of 75% of cilia GPCRs and 50% of the transition zone proteins were differentially expressed in SCZ. The present study is the first to draw associations between cilia and major psychiatric disorders, and is the first step toward understanding the role that cilia components play in their pathophysiological processes, which may lead to novel therapeutic targets for these disorders. DNA, the genetic material of most of the organisms, is the crucial element of life. Integrity of DNA needs to be maintained for transmission of genetic material from one generation to another. All organisms are constantly challenged by the environmental conditions which can lead to the induction of DNA damage. Ionizing radiation (IR) has been known to induce DNA damage and IR sensitivity varies among different organisms. The causes for differential radiosensitivity among various organisms have not been studied in great detail. We discuss DNA secondary structure formation, GC content of the genome, role of G-quadruplex formation, and its relationship with radiosensitivity of the genome. In Deinococcus radiodurans, the bacterium that exhibits maximum radio resistance, multiple G-quadruplex forming motifs are reported. In human cells, G-quadruplex formation led to differential radiosensitivity. In this article, we have discussed, the role of secondary DNA structure formation like G-quadruplex in shielding the genome from radiation and its implications in understanding evolution of radio protective effect of an organism. We also discuss role of GC content and its correlation with radio resistance. This review provides an insight into the role of G-quadruplexes in providing differential radiosensitivity at different site of the genome and in different organisms. It further discusses the possibility of higher GC content contributing towards reduced radiosensitivity in different organisms, evolution of radiosensitivity, and regulation of multiple cellular processes. This review provides an insight into the role of G-quadruplexes in providing differential radiosensitivity at different site of the genome and in different organisms. It further discusses the possibility of higher GC content contributing towards reduced radiosensitivity in different organisms, evolution of radiosensitivity, and regulation of multiple cellular processes. A serine/threonine kinase Pkc1 is the sole protein kinase C in the budding yeast Saccharomyces cerevisiae, and plays an important role in the regulation of polarized growth and stress responses such as those due to heat shock. Exposure of cells to high temperature transiently arrests polarized growth and leads to depolarization of the actin cytoskeleton, followed by actin repolarization during adaptation to heat shock stress. Actin repolarization is ensured by the activation of Pkc1 signaling; however, the molecular mechanisms underlying this phenomenon remain poorly understood. Using an overexpression construct of a constitutively active mutant of Pkc1 (Pkc1 ), we explored the Pkc1 target molecules involved in actin repolarization. PKC1 overexpression as well as heat shock stress increased the phosphorylation levels of Rho GTPase-activating protein (RhoGAP) Rgd1. Rgd1 was found to contribute to Pkc1-signaling-related actin repolarization during adaptation to heat shock stress in a GAP activity-independent manner, with Ser148 in Rgd1 playing a crucial role.