Epigallocatechin gallate-capped gold nanoparticles enhanced the tumor suppressors let-7a and miR-34a in hepatocellular carcinoma cells.

Epigallocatechin gallate (EGCG), major constituent of green tea, possesses antioxidant, antiviral, and anticancer activities. Gold nanoparticles (AuNPs) play an important role in drug delivery due to their stability, ease of surface functionalization, and unique optical properties. This study aimed to investigate the influence of EGCG-capped AuNPs on tumor suppressor miRNAs (miR-34a and let-7a) and their targeted cell death mediators in HepG2 cells, compared with celastrol. EGCG-AuNPs were prepared and characterized. antioxidant activity was estimated by DPPH scavenging assay; cytotoxicity was assessed by MTT assay; let-7a and miR-34a expression was analyzed by qPCR; and miRNAs targets (c-Myc and caspase-3) were assessed by ELISA and immunocytofluorescence, respectively. The average size of EGCG-AuNPs was 35 nm, with a λmax of ~535 nm. EGCG-AuNPs exerted cytotoxicity on HepG2 cells stronger than that of EGCG alone. EGCG-AuNPs and EGCG presented half-maximal radical scavenging concentrations (SC50) of 539 µg/ml and 45 µg/ml, respectively. The expression levels of let-7a and miR-34a were significantly elevated in HepG2 cells after EGCG-AuNP treatment for 72 h. c-Myc protein expression was reduced, whereas caspase-3 expression was increased following treatment with EGCG-AuNPs. In conclusion, Au-NPs are effective carrier for EGCG, and EGCG-AuNPs are promising anti-cancer agent.

Photodynamic therapy using 5-aminolevulinic acid triggered DNA damage of adenocarcinoma breast cancer and hepatocellular carcinoma cell lines.

Targeting cancer cells with photosensitizer (PS) excited by appropriate laser irradiation to release singlet oxygen as a photodynamic therapy (PDT) remains a challenge. This research aimed to assess the cytogenetic potential of 5-aminolevulinic acid (5-ALA) activated with laser irradiation (5-ALA/PDT) to damage the intact DNA of adenocarcinoma breast cancer cell line (MCF-7) and hepatocellular carcinoma cell line (HepG2). Cancer cells were treated with 0.5 and 1 mM 5-ALA for 4 h, the precursor of the photochemical protoporphyrin IX (PpIX), and then exposed to laser irradiation at 633 nm and 0.25 W for 4 min before incubation for 24 h. Cytotoxicity of cancer cells was assessed using trypan blue exclusion assay. Genotoxicity was recorded by micronucleus test and comet assay. Both 5-ALA and laser irradiation, separately, were nontoxic on cancer cell lines, however, 5-ALA/PDT enhanced cell death in a concentration-dependent manner. Also, 5-ALA/PDT generated high percentages of micronuclei in MCF-7 and HepG2 cell lines as recorded in binucleated cells. Similarly, the mean percentages of DNA damage and tail moment ratio were intensified extremely in cancer cell lines treated with 5-ALA/PDT rather than non-treated cells or cells treated by 5-ALA or laser irradiation separately. In conclusion, the singlet oxygen of 5-ALA targets DNA of cancer cells when activated by laser irradiation. Therefore, photodynamic therapy is an applicable process to damage DNA effectively during M-phase and prohibit cancer cells proliferation.