Proflavin suppresses the growth of human osteosarcoma MG63 cells through apoptosis and autophagy

Zhang, Mao‑Shu; Fuwen, Niu; Li, Kun

doi:10.3892/ol.2015.3206

Cited by 16 publications

(6 citation statements)

References 29 publications

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“…Autophagy and apoptosis are obviously different in terms of morphological or biochemical metabolic pathways, but there is a link between their functions. Due to interaction of apoptosis and autophagyrelated molecules, in some cases, autophagy and apoptosis can promote or antagonize each other [14,15]. Our results suggest that the proliferation rate of HeLa cell in 3-Ma and quercetin group is lower than that in quercetin alone group, indicating that inhibition of autophagy can increase the inhibition rate of HeLa cells.…”

Section: Discussioncontrasting

confidence: 57%

The critical role of quercetin in autophagy and apoptosis in HeLa cells

Wang

Zhang

et al. 2015

Tumor Biol.

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In recent years, the effects of quercetin on autophagy and apoptosis of cancer cells have been widely reported, while effects on HeLa cells are still unclear. Here, HeLa cells were subjected to quercetin treatment, and then proliferation, apoptosis, and autophagy were evaluated using MTT, flow cytometry, and MDC staining, respectively. The LC3-I/II, Beclin 1, active caspase-3, and S6K1 phosphorylation were detected using Western blot assay. The ultrastructure of HeLa was observed via transmission electron microscope (TEM). Our findings showed that quercetin can dose-dependently inhibit the growth of HeLa cells. The MDC fluorescence was enhanced with increased concentration of quercetin and hit a plateau at 50 μmol/l. Western blot assay revealed that LC3-I/II ratio, Beclin 1, and active caspase-3 protein were enforced in a dose-dependent method. However, the phosphorylation of S6K1 gradually decreased, concomitant with an increase of autophagy. In addition, TEM revealed that the number of autophagic vacuoles was peaked at 50 μmol/l of quercetin. Besides, interference of autophagy with 3-MA led to proliferation inhibition and increased apoptosis in HeLa cells, accompanied by the decreased LC3-I/II conversion and the increased active caspase-3. In conclusion, quercetin can inhibit HeLa cell proliferation and induce protective autophagy at low concentrations; thus, 3-MA plus quercetin would suppress autophagy and effectively increased apoptosis.

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Section: Discussioncontrasting

confidence: 57%

The critical role of quercetin in autophagy and apoptosis in HeLa cells

Wang

Zhang

et al. 2015

Tumor Biol.

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“…This finding is consistent with previous studies showing that allicin can induce autophagy in several cell types, such as thyroid cell lines [12] and human liver cancer cells [10]. It has been widely reported that there is a relationship between apoptosis and autophagy which underlies the process of cancer cell death [20,21].…”

Section: Gbm Is One Of the Most Incurable Forms Of Neoplasmssupporting

confidence: 93%

Allicin suppresses human glioblastoma cell growth by inducing cell cycle arrest and apoptosis, and by promoting autophagy

Weeranantanapan

Satsantitham

Sritangos

et al. 2020

ARCH BIOL SCI BELGRA

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Glioblastoma is the most aggressive cancer that occurs in the brain and spinal cord. In the present study, we investigated the effect of allicin, an organosulfur compound obtained from garlic (Allium sativum), on glioblastoma cell growth. When human glioblastoma DBTRG-05MG cells were incubated with different concentrations of allicin for 24 h, cell growth was suppressed in a dose-dependent manner. The results from image-based cytometer assays suggested that allicin caused S and G2/M phase cell cycle arrest and induced apoptosis. Autophagy detection studies showed that allicin also promoted this mechanism. Because cell migration is a key process during tumor formation, the effect of allicin on glioblastoma cell migration was also examined. After allicin treatment, the migration ability of cells decreased when compared with the control after 24 h. Taken together, the present results suggested that allicin inhibited human glioblastoma cell growth by inducing S and G2/M phase cell cycle arrest, apoptosis and autophagy. Our findings suggest that allicin suppressed glioblastoma cell growth through multiple target pathways. Therefore, allicin potentially serves as an alternative therapeutic candidate or could be synergistically used in combination with the standard drug for the treatment of glioblastoma multiforme.

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“…It has been demonstrated that autophagy play a protective role against neoplastic disease 48 and deregulation of autophagy is often implicated in several human diseases including cancers. Several studies have shown that tumor cells are defective in autophagy and/or apoptosis pathway.…”

Section: Discussionmentioning

confidence: 99%

Caprine herpesvirus 1 (CpHV-1) as a potential candidate for oncolytic virotherapy

Montagnaro

Damiano

Ciarcia

et al. 2018

Cancer Biology & Therapy

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Caprine Herpesvirus type 1 (CpHV-1) is a species-specific herpes virus able to induce apoptosis in several biological systems. In the present study we aimed to investigate the ability of CpHV-1 to reduce cells viability, to replicate and to cause cell death also in human cancer cell lines. We tested the CpHV-1 effects on HEL-299, Vero, MDA-MB-468, HeLa, U2OS, PC3, A549 and K562 neoplastic cell lines and on MDBK cells. Firstly, we evaluated the effect of CpHV-1 infection on cell viability by MTT assay and our data showed that CpHV-1 can induce a marked cytopathic effect (CPE) in most of cell lines tested, except for HEL-299, Vero and K562 cells. The reduction of cell viability was associated with a significant increase of viral production. We next investigated if CpHV-1 was able to induce cell death and so through western blotting analysis we evaluated cleaved caspase 3, LC3II and p62 protein levels after infection. Caspase 3 activation was detected in MDBK cells and, even if at different times p.i., also in MDA-MB-468, U2OS, and PC3 cell lines, while LC3II increase and concomitant p62 protein reduction were observed only in U2OS, and A549 cells, no significant alteration of these proteins was observed in the other cell lines tested. Finally, to confirm virus ability to trigger apoptosis we performed an Annexin-V apoptosis test after 24 h p.i. Although we need to further explore mechanisms underlying CpHV-1 treatment, this study could serve as the basis for the development of new treatment options aiming to fight several cancer types.

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Proflavin suppresses the growth of human osteosarcoma MG63 cells through apoptosis and autophagy

Cited by 16 publications

References 29 publications

The critical role of quercetin in autophagy and apoptosis in HeLa cells

The critical role of quercetin in autophagy and apoptosis in HeLa cells

Allicin suppresses human glioblastoma cell growth by inducing cell cycle arrest and apoptosis, and by promoting autophagy

Caprine herpesvirus 1 (CpHV-1) as a potential candidate for oncolytic virotherapy

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