Flavones inhibit the proliferation of human tumor cancer cell lines by inducing apoptosis

Abstract

Dietary flavonoids have been shown to exert specific cytotoxicity toward some cancer cells, but the precise molecular mechanisms are still not completely understood. In this study, cytotoxic effects of flavones (apigenin and luteolin) on two different cancer cell lines, including human chronic myelogenous erythroleukaemia (K562) and bladder carcinoma (RT112), were determined, and the molecular mechanisms responsible for their cytotoxic effects were studied. The results of an MTT assay showed that luteolin and apigenin were able to induce cytotoxicity in K562 and RT112 cells in a dose- and time-dependent manner. The cytotoxic potency of luteolin was higher than that of apigenin. Flow-cytometry and DNA-fragmentation analysis indicated that the cytotoxicity induced by luteolin and apigenin was mainly due to apoptosis, with minor cell-cycle perturbations. This apoptotic response was characterized by an increase of the sub-G1 fraction of treated cells, poly(ADP-ribose) polymerase proteolysis, typical ladder of DNA fragmentation, and Annexin V-positive cells. In conclusion, luteolin and apigenin exert cytotoxic effects in different cancer cell lines in which apoptosis plays an important role. Thus, flavones could be considered as potential chemotherapeutic agents.

Green synthesis palladium nanoparticles mediated by white tea (<em>Camellia sinensis</em>) extract with antioxidant, antibacterial, and antiproliferative activities toward the human leukemia (MOLT-4) cell line

“…39 The anticancer effects of flavonoids occur through oxidative destruction, inhibition of proliferation, inactivation of carcinogen, promotion of differentiation, induction of cell-cycle arrest and apoptosis, impairment of tumor angiogenesis, and suppression of metastasis. [40][41][42] Flavonoids can interact with xenobiotic metabolizing enzymes and inhibit involvement of kinases signal transduction, interact with estrogen type II binding sites, and alter gene expression patterns, 43,44 with resultant promotion of antiproliferative activity of Pd@W.tea NPs.…”

Cytotoxicity of Mycobacterium indicus pranii on Mia-Pa-Ca2 cells

“…Drugs like gemcitabine and 5-FU remain the standard of care for pancreatic cancer [28], even though it has been almost decades since they were established. Similar to our findings on Mia-Pa-Ca2 cells, previous in-vitro studies reported that treatment of human pancreatic adeno-carcinoma cells (Mia-Pa-Ca2, AsPC-1, Panc-1, and Panc-48) and also of patients with advanced pancreatic cancer with gemcitabine [29,30] and 5-FU [31,32] inhibited cell growth in a dose-dependent manner [33].…”

Cytotoxicity of dietary flavonoids on different human cancer types

“…[6667] Mitigation of oxidative damage, inactivation of carcinogen, inhibition of proliferation, promotion of differentiation, induction of cell cycle arrest and apoptosis, impairment of tumor angiogenesis, and suppression of metastasis contribute to the anticarcinogenic activities of flavonoids. [242530324968] These polyphenolic compounds can interact with xenobiotics metabolizing enzymes, inhibit several kinases involved in signal transduction, interact with estrogen type II binding sites, and alter gene expression patterns. [61697071]…”

“…[26] Strong and consistent epidemiological evidences suggest that a diet enriched with naturally occurring substances significantly reduces the risk for many cancers. [2728293031] Indeed, the adoption of diets rich in vegetables and fruits, together with the maintenance of physical activity and appropriate body mass, could reduce the cancer incidence by 30-40%. [323334] Moreover, several studies suggest that there is a decreased risk for different types of cancer among vegetarians.…”