Schizandrin A exerts anti-tumor effects on A375 cells by down-regulating H19

Bi, Ye; Fu, Yan; Wang, Shuyan; Chen, Xingxiu; Cai, Xiaoping

doi:10.1590/1414-431x20198385

Cited by 11 publications

(10 citation statements)

References 34 publications

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“…Moreover, the migration and invasion of AGS cells were both decreased after SchA treatment, and SchA at the concentration of 30 µM exerted the most obvious inhibitory effects on the migration and invasion of AGS cells. Furthermore, the apoptosis of AGS cells was significantly induced by SchA, which was in line with previous findings suggesting the promoting role of SchA in the apoptosis of human cancer cells (7).…”

Section: Discussionsupporting

confidence: 92%

“…Additionally, it can promote the cell cycle arrest, apoptosis and cell death induced by heat shock transcription factor 1, thereby impeding the proliferation of colorectal cancer cells (6). SchA can obstruct the proliferation and invasion of melanoma cells and the phosphorylation of PI3K/AKT by repressing H19 imprinted maternally expressed transcript expression (7). In addition, it can modulate the overactivation of Wnt and activate endoplasmic reticulum (ER) stress to induce the cell cycle arrest and apoptosis of triple-negative breast cancer cells (4).…”

Section: Introductionmentioning

confidence: 99%

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Schizandrin A induces the apoptosis and suppresses the proliferation, invasion and migration of gastric cancer cells by activating endoplasmic reticulum stress

Qian

Wang³

et al. 2021

Mol Med Rep

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Apart from its basic antioxidant and anti-inflammatory properties, schizandrin A (SchA), which is isolated from Fructus schisandra, can exert anticancer effects on multiple cancer types. However, to the best of our knowledge, there has been no study identifying the impacts of SchA on gastric cancer (GC). Therefore, the aim of the present study was to identify how SchA functioned to affect the progression of GC. To investigate the role of SchA in GC development, Cell Counting Kit-8, colony formation, wound healing and Transwell assays were conducted to assess the viability, proliferation, migration and invasion of AGS cells, respectively. Then, the apoptosis rate and apoptosis-and endoplasmic reticulum (ER) stress-related protein expression levels in AGS cells exposed to SchA were detected via TUNEL assays and western blotting, respectively. Subsequently, the aforementioned functional assays were performed again in AGS cells exposed to both SchA and the ER stress inhibitor 4-phenylbutyric acid (4-PBA) for the confirmation of the effect of SchA on ER stress in GC. It was found that SchA markedly decreased the viability, proliferation, migration and invasion, while it induced the apoptosis of AGS cells. Moreover, the markers of ER stress were elevated by SchA treatment in AGS cells. Nevertheless, 4-PBA reversed the effects of SchA on the viability, proliferation, migration, invasion and apoptosis of AGS cells, accompanied by decreased expression of ER stress markers. In conclusion, the present study demonstrated that SchA induced the apoptosis and suppressed the proliferation, invasion and migration of GC cells by activating ER stress, which provides a theoretical basis for the use of SchA in the treatment of GC.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Schizandrin A induces the apoptosis and suppresses the proliferation, invasion and migration of gastric cancer cells by activating endoplasmic reticulum stress

Qian

Wang³

et al. 2021

Mol Med Rep

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“…H19 has been reported to regulate autophagy in various types of cancer, and its aberrant expression was associated with tumorigenesis. 38,39 The role of H19 in periodontitis has not been investigated previously. In the present study, we determined the expression of H19 in PDLCs under TNFα and LPS stimulation as well as in inflamed periodontal tissue.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Non-Coding RNA H19 Participates in Periodontal Inflammation via Activation of Autophagy</p>

Guo

Huang

Líu

et al. 2020

JIR

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Purpose: Periodontitis is the leading cause of tooth loss. The role of long non-coding RNA (lncRNA) in periodontal inflammation remains unclear. The aim of this study was to investigate the role of lncRNA H19 in periodontitis and its possible regulation of autophagy in periodontitis. Material and Methods: Inflammation level was determined by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) in periodontal ligament cells (PDLCs). Western blotting, flow cytometric analysis, and immunofluorescence staining were used to detect the autophagy flux. Overexpression or knockdown of H19 was used to confirm its function. Ligature-induced periodontitis model in mice and periodontitis-affected human gingival tissue were used in vivo. RNA sequencing was performed to determine the differentially expressed genes. Results: Autophagy was significantly increased in PDLCs after inflammatory stimulation as well as in a ligature-induced periodontitis model in mice and periodontitis-affected human gingival tissue. During the inflammatory process, H19 expression was also significantly upregulated. Further, the levels of autophagic markers were significantly upregulated after overexpressing H19 in PDLCs, and the increased autophagic activity induced by inflammatory stimulation was reversed by H19 knockdown. RNA sequencing showed that the expression profiles of mRNAs were significantly altered after H19 overexpression, and the differentially expressed genes were enriched in the PI3K/AKT signaling pathway, which was confirmed by the decreased p-AKT protein expression in the H19 overexpression group. Conclusion: Periodontal inflammation activates autophagy flux, and H19 mediates the activation of autophagy via AKT pathway in periodontitis. This study expands our understanding of molecular regulation in periodontitis.

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“…Over the past decade, studies investigating the potential antitumor effects of SchA have been gradually increasing. It was previously reported that SchA can inhibit cell proliferation, induce cell apoptosis, inhibit cell invasion and tumor metastasis in breast cancer, ovarian cancer, choriocarcinoma, thyroid cancer and colorectal cancer (31,(35)(36)(37)(38)(39)(40)(41)(42), in addition to enhancing drug efficacy in NSCLC and colon carcinoma (43,44) or overcome drug resistance in breast cancer and esophageal carcinoma (30,45,46). In particular, Xian et al revealed that SchA combined with gefitinib could inhibit proliferation whilst promoting apoptosis in gefitinib-resistant NSCLC cells (43).…”

Section: Schizandrin a Can Inhibit Non-small Cell Lung Cancer Cell Proliferation By Inducing Cell Cycle Arrest Apoptosis And Autophagymentioning

confidence: 99%

Schizandrin A can inhibit non‑small cell lung cancer cell proliferation by inducing cell cycle arrest, apoptosis and autophagy

Zhu

Wang

et al. 2021

Int J Mol Med

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Schizandrin A (SchA) can be extracted from the vine plant Schisandra chinensis and has been reported to confer various biologically active properties. However, its potential biological effects on non-small cell lung cancer (NSCLC) remain unknown. Therefore, the present study aims to address this issue. NSCLC and normal lung epithelial cell lines were first treated with SchA. Cell viability and proliferation were measured using CellTiter-Glo Assay and colony formation assays, respectively. PI staining was used to measure cell cycle distribution. Cell cycle-related proteins p53, p21, cyclin D1, CDK4, CDK6, cyclin E1, cyclin E2, CDK2 and DNA damage-related protein SOX4 were detected by western blot analysis. Annexin V-FITC/PI staining, DNA electrophoresis and Hoechst 33342/PI dual staining were used to detect apoptosis. JC-1 and DCFH-DA fluorescent dyes were used to measure the mitochondrial membrane potential and reactive oxygen species concentrations, respectively. Apoptosis-related proteins caspase-3, cleaved caspase-3, poly(ADP-ribose) polymerase (PARP), cleaved PARP, BimEL, BimL, BimS, Bcl2, Bax, caspase-9 and cleaved caspas-9 were measured by western blot analysis. Dansylcadaverine was used to detect the presence of the acidic lysosomal vesicles. The expression levels of the autophagy-related proteins LC3-I/II, p62/SQSTM and AMPKα activation were measured using western blot analysis. In addition, the autophagy inhibitor 3-methyladenine was used to inhibit autophagy. SchA treatment was found to reduce NSCLC cell viability whilst inhibiting cell proliferation. Low concentrations of SchA (10-20 µM) mainly induced G 1 /S-phase cell cycle arrest. By contrast, as the concentration of SchA used increases (20-50 µM), cells underwent apoptosis and G 2 /M-phase cell cycle arrest. As the treatment concentration of SchA increased from 0 to 50 µM, the expression of p53 and SOX4 protein also concomitantly increased, but the expression of p21 protein was increased by 10 µM SchA and decreased by higher concentrations (20-50 µM). In addition, the mRNA and protein expression levels of Bcl-like 11 (Bim) EL, BimL and BimS increased following SchA application. SchA induced the accumulation of acidic vesicles and induced a marked increase in the expression of LC3-II protein, suggsting that SchA activated the autophagy pathway. However, the expression of the p62 protein was found to be increased by SchA, suggesting that p62 was not degraded during the autophagic flux. The 3-methyladenine exerted no notable effects on SchA-induced apoptosis. Taken together, results from the present study suggest that SchA exerted inhibitory effects on NSCLC physiology by inducing cell cycle arrest and apoptosis. In addition, SchA partially induced autophagy, which did not result in any cytoprotective effects.

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Schizandrin A exerts anti-tumor effects on A375 cells by down-regulating H19

Cited by 11 publications

References 34 publications

Schizandrin A induces the apoptosis and suppresses the proliferation, invasion and migration of gastric cancer cells by activating endoplasmic reticulum stress

Schizandrin A induces the apoptosis and suppresses the proliferation, invasion and migration of gastric cancer cells by activating endoplasmic reticulum stress

<p>Long Non-Coding RNA H19 Participates in Periodontal Inflammation via Activation of Autophagy</p>

Schizandrin A can inhibit non‑small cell lung cancer cell proliferation by inducing cell cycle arrest, apoptosis and autophagy

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