Artesunate promotes sensitivity to sorafenib in hepatocellular carcinoma.

Enhancing sensitivity of carcinoma to sorafenib (Sor) is critical to overcome the limits of high frequency resistance and moderate efficiency during chemotherapy for advanced hepatocellular carcinoma (HCC). Here, we promote sensitivity of HCC to Sor by combination with Artesunate (Art), a derivative of artemisinin extracted from Chinese medical herb. The positive synergy of Art on inhibiting HCC growth contributes 48% dosage of Sor to reduce tumor cell viability in vitro and tumor size in vivo.

Dependence of artesunate on long noncoding RNA-RP11 to inhibit epithelial-mesenchymal transition of hepatocellular carcinoma.

As a first line medicine for malaria treatment, artesunate (ART) also shows antitumor potential. However, little is known about the effect of ART on the cancer cell epithelial-mesenchymal transition (EMT). In this study, we found that ART inhibited cell growth in SK-HEP1 and SM7721 hepatocellular carcinoma cell lines.

[ESAT-6 inhibits autophagy in macrophages and promotes the growth of BCG].

Objective To explore the interaction between 6 kD early secretory antigenic target (ESAT6) and autophagy in order to provide an experimental basis for the immune evasion mediated by ESAT6. Methods RAW264.7 cell lines (mouse macrophages) were treated with Earle's balanced salt solution (EBSS), and another cells were transfected by control plasmid pCMV-HA or recombinant plasmid pCMV-HA-ESAT6.

[SapM-induced fusion blocking of autophagosome-lysosome is depended on interaction with Rab7].

Objective To study the role of Rab7 in the blockage of autophagosome-lysosome fusion induced by secretory acid phosphatase (SapM), a virulence factor of mycobacterium tuberculosis. Methods The Raw264.7 cells were transfected with siRab7, and the P62 was detected using Western blotting.

[Secretory acid phosphatase of Mycobacterium tuberculosis inhibits the autophagy of murine macrophages].

Objective To investigate the effect of secretory acid phosphatase as a virulence factor of Mycobacterium tuberculosis (SapM) on the autophagy of murine macrophages. Methods GFP-LC3-Raw264.7 cells were treated with SapM, wortmannin, or starvation.

ESAT6 inhibits autophagy flux and promotes BCG proliferation through MTOR.

In recent years, increasing studies have found that pathogenic Mycobacterium tuberculosis (Mtb) inhibits autophagy, which mediates the anti-mycobacterial response, but the mechanism is not clear. We previously reported that secretory acid phosphatase (SapM) of Mtb can negatively regulate autophagy flux. Recently, another virulence factor of Mtb, early secretory antigenic target 6 (ESAT6), has been found to be involved in inhibiting autophagy, but the mechanism remains unclear.

[Establishment of RAW264.7 cell strain stably expressing RFP-GFP-LC3].

Objective: To establish murine macrophage RAW264.7 cell strain with stable expression of red fluorescent protein-green fluorescent protein-microtubule associated protein light chain 3 (RFP-GFP-LC3).

Methods: A lentiviral vector containing RFP-GFP-LC3 gene was constructed and then packaged in HEK293T cells with the packaging plasmids.

Autophagy regulation revealed by SapM-induced block of autophagosome-lysosome fusion via binding RAB7.

The mechanism underlying autophagy alteration by mycobacterium tuberculosis remains unclear. Our previous study shows LpqH, a lipoprotein of mycobacterium tuberculosis, can cause autophagosomes accumulation in murine macrophages. It is well known that SapM, another virulence factor, plays an important role in blocking phagosome-endosome fusion.