The current study evaluated the anti-cancer properties of bio-functionalized silver nanoparticles fabricated by Juniperus chinensis leaf extracts. The nanoparticles were characterized by scanning electron microscopy, transmission electron microscopy, UV–visible spectroscopy, Fourier transform infrared spectroscopy, X-ray diffraction, dynamic light scattering, Zeta potential and X-ray spectroscopy. Further, this study elucidated the cellular and molecular mechanisms of nanoparticles for anti-proliferative and apoptotic effects on human lung cancer cells (A549) and compared them with commercial drug cisplatin. The size of the spherical nanoparticle was 12.96 nm with negative zeta potential. Up-regulation of caspase 3,9 and p53, Annexin V-FITC/PI, DAPI staining, and ROS production indicated the remarkable apoptotic effect of AgNPs compared to cisplatin. Moreover, down-regulation of MMP2/MMP9 scratch and matrigel assays revealed anti-metastatic properties of AgNPs. Cell cycle analysis and downregulation of cyclin D1 indicated cancer cell cessation in the G0/G1 phase. Overall, the results revealed that the green-synthetized AgNPs had anti-metastasis and anti-proliferation effects on lung cancer cells in comparison to cisplatin with lower side effects on the normal cell line.

The current study reveals anti-cancer properties of bio-functionalized silver nanoparticle (AgNPs) fabricated by Juniperus chinensis leaf extracts due to it’s easy, low cost, biological activity, eco-friendly and lower side effects. The characteristics of AgNPs were determined by scanning electron microscopy [1], transmission electron microscopy (TEM), UV-visible spectroscopy, Fourier transform infrared (FTIR) spectroscopy, X-ray diffraction, Dynamic light scattering (DLS), Zeta potential and X-ray spectroscopy (EDX). Further, this study highlights the cellular and molecular mechanisms of AgNPs involves in anti-proliferative and apoptotic effect on human lung cancer cells (A549) and compared to commercial drug cisplatin by various biological methods such as MTT, flow cytometery analysis, gene expression patterns, migration and invasion inhibition, ROS and caspase production and cell staining. The size of AgNPs fabricated in this study was 12.96 with spherical shape and negative zeta potential. Up-regulation of capase 3,9 and p53, Annexin V-FITC/PI, DAPI staining, ROS production indicated remarkable apoptotic effect of AgNPs than cisplatin. Also down-regulation of MMP2/MMP9 scratch and matrigel assays revealed anti-metastatic properties of AgNPs.cell cycle analysis and down regulation of cyclin D1 showed cancer cell cessation in the G0/G1 phase. Overall results in current experiment revealed AgNPs synthetized by biogreen method anti-metastasis and anti-proliferation effect on lung cancer cells comparison to cicplatin drug and also had lower side effect on normal cell line.

Background: Wogonin as a flavonoid compound is known for its anticancer effect through growth control, differentiation, and apoptosis. This study investigates the possible activity of wogonin in inducing cell death of breast tumors MDA-MB231. Materials and Methods: The level of cell proliferation was evaluated by MTT assay. Cycle analysis and the apoptotic rate were assessed by flow cytometry. mRNA level of Bax, Bcl-2, p53, and survivin was evaluated by real-time PCR. Western blot was utilized to assert the relative protein expression. Results: Wogonin inhibits the proliferation of MDA-MB231 over time, and in particular, wogonin can induce the arrest of phase G1 of MDA-MB231 cells. The apoptosis of wogonin was related to a remarkable decrease in Bcl-2 and survivin and an increment in p53 and Bax. Wogonin also significantly elevated the active apoptotic forms of caspase-3, -8, -9. Z-DEVD-FMK, a specific inhibitor of caspase-3, remarkably inhibits cellular apoptosis caused by wogonin. Wogonin suppresses PI3K/Akt phosphorylation and ERK-derived phosphorylation. PD98059, a specific ERK inhibitor, significantly blocked the apoptosis caused by wogonin. Also, LY294002, a specific suppressor of PI3K, remarkably elevates the cellular apoptosis caused by wogonin. Various studies demonstrated that LY294002 not only modulates the expression of the survivin gene alone but also enhances the suppression of the expression of survivin with wogonin. Conclusion: The apoptotic role of wogonin is observed by the triggering caspases and ERK and is associated with the suppressive pathways of the PI3K/Akt/survivin signal in the MDA-MB231 cells.

Background: Colorectal cancer (CRC) has already been considered the fourth leading cause of mortality worldwide as the genes involved in apoptotic pathways and alterations of reversible epigenetic have an important role in the progression of CRC. Objectives: The current study aimed to evaluate the effect of sodium butyrate as a histone deacetylase inhibitor on the alterations of the gene expression of FAS, Fas ligand (FASL), Death receptor 4 in HCT-116 CRC cell line. Methods: HCT-116 cell line was cultured in Dulbeccoʼs Modified Eagle Medium. The cytotoxicity effect of sodium butyrate on HCT-116 was evaluated using 3-(4, 5-dimethylthiazol-2-yl)-2, 5- diphenyltetrazolium bromide assay for three incubation times (i.e., 24, 48, and 72 h). The half-maximal inhibitory concentration (IC50) values were determined. The optimum concentration was within the range of 6.25-200 mM. The cellular ribonucleic acid was extracted, and complementary deoxyribonucleic acid was synthesized. Finally, the alterations of the gene expression of FAS, FASL, DR4, DR5, and TRAIL were assessed by real-time polymerase chain reaction (PCR). Results: The IC50 levels for three incubation times were 50, 12.5, and 6.25 mM, respectively. The obtained results of real-time PCR demonstrated a significant increase in the gene expression of TRAIL, DR5, and FAS in comparison to that of the untreated cells as the control group at the three incubation times. The DR4 gene expression significantly increased in comparison to that reported for the control group at 48 and 72 h of incubation. In addition, FASL gene expression remarkably decreased at the three incubation times. Conclusions: Sodium butyrate could show cytotoxicity effect on CRC cell lines through the induction of death receptors in the extrinsic apoptotic pathway. The obtained results of this study revealed that the optimum effect of sodium butyrate is an incubation time-dependent and concentration-dependent manner.