ABSTRACT
Objective: To research the effect of matrine on the proliferation and migration of HepG2 cells through extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. Methods: HepG2 cell was selected and divided into blank control group, experimental group (matrine 1, 2, and 4 mg/mL), and positive control group (PD98059, ERK1/2 inhibitor). MTT measure was used to detect the effective time and concentration which matrine inhibits HepG2 cells. After 24 h, the effect of effective concentration of matrine on the of morphological changing HepG2 cells was observed. The invasion ability was assayed by transwell method, the expression of ERK1/2 and pERK1/2 were detected through Western blot, and reverse transcription polymerase chain reaction was used to test the expression level of ERK1/2 mRNA. Results: With the increase of matrine concentration, the number of adherent HepG2 cells gradually decreased, the morphologic changes gradually became spherical, some cell morphology was incomplete, and even cell fragments appeared. The proliferation and invasion ability of HepG2 cells decreased. The expression of ERK1/2, pERK1/2, and ERK1/2 mRNA downregulated with the increase of matrine concentration (P < 0.05). Conclusion: Matrine inhibits the proliferation and migration of HepG2 cells by downregulating the ERK1/2 signaling pathway.
ABSTRACT
Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with quick disease progression and poor prognosis. The pathogenesis is extremely complex, involving genetic mutations, abnormal activation of signal pathways, and epigenetic changes. Autophagy is a basic physiological phenomenon of maintaining internal environment stability and promoting cell survival when cell stress occurs, which plays an important role in the occurrence, development and prognosis of various tumors including HCC. Autophagy can participate in the formation and progress of HCC through the above molecular mechanisms. This paper reviews the progress of relationship between autophagy and HCC.