Bioleaching is one of the well-known methods of metal recovery with Environmental benefits. This process has been extensively used for combating improper waste management issues along with metal reclamation. The aim of this study is to bioleach spent petroleum refinery catalyst at variant pulp densities (PD) (5, 10 and 15%) using microorganisms in acidic pH (1.5-1.6) and mesophilic temperature (30-35 °C). The study includes leaching yields of metals like nickel, molybdenum, copper and aluminum. The three bioleaching experiments with different pulp densities yielded a maximum of more than 90% nickel, 73% copper, 87% molybdenum and 24% aluminum. The results are validated 5, 10, and 15% pulp density and the result is validated with pH, Redox potential, microbial population, sulphate concentration and ferrous iron, concentration. The time saving due to faster nickel dissolution using iron and sulphur oxidizing microorganisms would be economical for the bioleaching process.Present study aims to investigate the combined effect of anticancer drug, norcantharidin (NCTD) in combination with glycolytic inhibitor, i.e. 2-deoxy-d-glucose (2-DG) in liver cancer (HepG2 and Hepa 1-6) cells. Cell viability of NCTD and 2-DG exposed cells was determined by MTT assay, whereas, colony-forming efficiency and migration rate was determined by clonogenic assay and wound healing assay, respectively. Nuclear DAPI staining and Annexin V FITC-PI staining were used to study the apoptosis induction in cells. Fluorescence microscopy imaging was performed to detect the intracellular reactive oxygen species (ROS) generation and mitochondrial membrane potential by staining with DCFDA and JC-1 dye, respectively. Cell viability assay revealed that NCTD and 2-DG exposure in combination displays more cytotoxic effect than a single drug. Additionally, cells lose their colony formation efficiency, as well as the reduced migration rate ability was also observed upon combined exposure. Increased nuclear condensation and mitochondrial membrane depolarization are considered as key features for apoptosis induction in cancerous cells. Furthermore, oxidative stress produced in cells due to enhanced intracellular ROS generation is also major probability for cellular damage. Thus, from the initial data it can be concluded that further preclinical studies will be needed to prove the efficacy of NCTD and 2-DG in hepatocellular carcinoma therapy.Lung cancer is one of the leading causes of cancer deaths worldwide and existing approaches are not enough to manage, and hence, it is important to concentrate on new drug strategies. This study was aimed to identify the interacting partner of Flap endonuclease 1 (FEN1) and its role in cancer treatment. We identified a new FEN1 interacting partner confirmed it as Heat Shock Protein 70 (HSP 70), and its effect on FEN1 expression, in vitro. Additionally, we found that the 5-Fluorouracil's (5-FU) function was significantly improved when used in combination with HSP 70 inhibitor (KNK 437). https://www.selleckchem.com/products/hg-9-91-01.html The findings are interesting, elucidating the synergistic mechanism between two compounds which helps to develop a novel management strategy for over-expressed FEN1 in the lung. The online version contains supplementary material available at 10.1007/s13205-020-02598-3. The online version contains supplementary material available at 10.1007/s13205-020-02598-3.In this study, a suicide gene therapy approach was optimized by a non-viral polyplex system based on pEGFP-N1 vector harboring purine nucleoside phosphorylase gene conducted by vascular endothelial growth factor promoter for an in vitro breast cancer model (4T1 cell line). The VEGF promoter and purine nucleoside phosphorylase gene were cloned into the vector from the source of 4T1 and E. coli genomic DNA, respectively. A gene construct was developed by replacing VEGF promoter instead of CMV promoter in pEGFP-N1vector. PNP gene was integrated in to the multiple cloning site of the obtained vector. On the other hand, a construct from pEGFP-N1 harboring PNP gene under the control of the original CMV promoter was developed. The transfection method using cationic polymer was optimized based on N/P ratio, cell cytotoxicity, polyplex size, zeta potential and the green fluorescent protein (GFP) expression by fluorescent microscopy and flowcytometry. Also, the effect of hypoxia condition induced by 0.5 mM H2O2 on the promoter efficiency was investigated. The results showed that the performed gene delivery system is capable of the gene transfection to more than 30% of the cancer cells with both VEGF-PNP-pEGFP-N1 and PNP-pEGFP-N1 plasmids. The hypoxia condition did not show a significant effect on the VEGF promoter. But, it revealed that bystander effect can improve the efficacy of this system and reduce drug IC50 to 2 and fourfold for plasmids VEGF-PNP-pEGFP-N1 and PNP-pEGFP-N1, respectively. These results showed that the bystander effect could almost compensate the low efficiency of non-viral gene delivery systems. We suggest that the tumor-specific gene expression system mediated by the VEGF promoter can be especially useful in the present model of breast cancer gene therapy.The G protein-coupled receptors (GPRs) have been shown to regulate several cancer related processes. The aberrant expression of GPRs has been linked to the development of several cancers. The present study was designed to examine the expression and decipher the role of GPR15 in the development of human colorectal cancer. The results revealed GPR15 to be significantly (P  less then  0.05) upregulated in colorectal cancer cells. The silencing of GPR15 inhibited the growth of the colorectal cancer cells via induction of apoptosis. Induction of apoptosis in colorectal cancer cells was associated increase in Bax and decrease in Bcl-2 expression. The silencing of GPR-15 also caused a significant (P  less then  0.05) decline in the migration and invasion of the colorectal cancer cells. Bioinformatic analysis and luciferase assay revealed that the expression of GPR15 to be post-transcriptionally regulated by microRNA-1225 (miR-1225). The expression of miR-1225 was found to significantly (P  less then  0.05) downregulated in colorectal cancer cells and its overexpression caused suppression of GPR15 and inhibited the proliferation of the colorectal cancer cells.