<i>Retracted:</i> Sinomenine exerts antitumour effect in gastric cancer cells via enhancement of miR‐204 expression

Yuan, Haifeng; Zhang, Jinghua; Li, Fuli; Li, Wei; Wang, Haichao

doi:10.1111/bcpt.13285

Cited by 16 publications

(16 citation statements)

References 35 publications

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“…As expected, sinomenine can affect the growth and apoptosis of RB cells in vitro; moreover, sinomenine also lead to decreased migration as well as invasion ability of the RB cells, and the effects of sinomenine were in a dose-dependent manner. These results were consistent with its anti-tumor behaviors in other cancers 9,[12][13][14] . Like any other type of cancer cell, RB cells 7,18) were characterized by the uncontrolled growth and increased migration and invasion ability of the tumor cells, the above observations suggested that sinomenine can inhibit the growth and metathesis of WERI-RB-1 and Y79 cells in vitro, suggesting that sinomenine can exert anti-tumor effects in RB.…”

Section: Effect Of Sinomenine Treatment On the Migration As Well As Isupporting

confidence: 87%

“…In clinical field, sinomenine has been proved to play protective roles in cardiovascular system, immune system, as well as other tissues and organs 10,11) . So far, sinomenine has been regarded as an anti-tumor reagent for the treatment of many types of cancers, for example, gastric cancer, breast cancer and so on [12][13][14] . However, the roles as well as underlying mechanisms of sinomenine in regulating the progression of RB has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Sinomenine Can Inhibit the Growth and Invasion Ability of Retinoblastoma Cell through Regulating PI3K/AKT Signaling Pathway

Zheng

Zhu

et al. 2020

Biological & Pharmaceutical Bulletin

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Sinomenine was found to play anti-cancer functions in different type of cancers, while the mechanisms underlying the anticancer effects of sinomenine in retinoblastoma (RB) remains unclear. The present study was designed to explore the impacts of sinomenine on cell proliferation and invasion ability of RB cells and the related mechanism. Human retinoblastoma cell line WERI-RB-1 and Y79 cells were cultured and treated by different concentration of sinomenine, and then the proliferation ability of the cells was determined via performing the MTT proliferation assay. The cell apoptosis was examined via performing the flow cytometry assay. Then scratch wound healing analysis as well as and transwell invasion analysis have been performed to determine the effect of sinomenine on cell migration ability as well as invasion ability. The proteins level of PI3K/AKT signaling molecules were determined with western blot assay. We found that sinomenine was able to decrease the proliferation and promote the apoptosis of RB cells in a dose-dependent manner; moreover, sinomenine also significantly suppressed the migration as well as invasion ability of WERI-RB-1 and Y79 cells in vitro. Furthermore, sinomenine also deactivated PI3k/AKT signaling in WERI-RB-1 cells via inhibited the phosphorylation of PI3K and AKT proteins. Sinomenine can exert anti-tumor function on RB cells in vitro, therefore sinomenine might be a potential alterative medication for the treatment for RB.

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Section: Effect Of Sinomenine Treatment On the Migration As Well As Isupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Sinomenine Can Inhibit the Growth and Invasion Ability of Retinoblastoma Cell through Regulating PI3K/AKT Signaling Pathway

Zheng

Zhu

et al. 2020

Biological & Pharmaceutical Bulletin

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“…Cyclin D1 has been recognized as a proto-oncogene to promote cell cycle from G1 phase to S phase by activating CDK4, a cyclin-dependent kinase specific to G1 phase. Some studies have reported that AMPK inhibits GC growth via cyclin D1 suppression [41,60]. As is known, the metastasis is a crucial characteristic for the late stages of cancer [42,61].…”

Section: Discussionmentioning

confidence: 99%

The role of TRPV1 ion channels in the suppression of gastric cancer development

Gao

Yang

Chen

et al. 2020

J Exp Clin Cancer Res

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Background Although the aberrant expression and function of most Ca2+-permeable channels are known to promote gastrointestinal tumors, the association between transient receptor potential vanilloid receptor 1 (TRPV1) channels and gastric cancer (GC) has not yet been explored. Herein, we sought to determine the role of TRPV1 channels in the development of GC and to elucidate the underlying molecular mechanisms involved therein. Methods Immunohistochemistry, qPCR, Western blot, immunofluorescence assays were used to detect the mRNA and protein expression of TRPV1 in GC cells and tissues, and the clinical significance of TRPV1 in GC was also studied by clinicopathologic analysis. CCK8, colony formation, flow cytometry assays were used to detect the proliferation and survival of GC cells, while transwell assay was used to detect migration and invasion of GC cells in vitro. Tumor xenograft and peritoneal dissemination assays in nude mice were used to examine the role of TRPV1 in GC development in vivo. Results TRPV1 expression was significantly downregulated in human primary GC tissues compared to their adjacent tissues. The decreased expression of TRPV1 proteins in GC tissues was positively correlated with tumor size, histological grade, lymphatic metastasis, clinical stage, and was strongly correlated with poor prognosis of GC patients. Moreover, the expression of TRPV1 was closely correlated with Ki67, VEGFR, and E-cadherin, all of which are the well-known cancer markers for proliferation and metastasis. TRPV1 proteins were predominately expressed on the plasma membrane in several GC cell lines. TRPV1 overexpression blocked cell cycle at G1 phase to inhibit GC cell proliferation and attenuated migration and invasion of GC cells in vitro, but TRPV1 knockdown increased these parameters. TRPV1 significantly reduced gastric tumor size, number and peritoneal dissemination in vivo. Mechanistically, TRPV1 overexpression in GC cells increased [Ca2+]i, activated CaMKKβ and AMPK phosphorylation, and decreased expression of cyclin D1 and MMP2, while TRPV1 knockdown induced the opposite effects. Conclusions TRPV1 uniquely suppresses GC development through a novel Ca2+/CaMKKβ/AMPK pathway and its downregulation is correlated with poor survival of human GC patients. Thus, TRPV1 upregulation and its downstream signaling may represent a promising target for GC prevention and therapy.

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“…The anti-tumor activity of sinomenine was well studied in gastric, 21,22 breast, 23 prostate, 24 cervical 25 cancer, renal cell carcinoma, 26 and glioma. 27 Inhibition of cell cycle progression, 27 angiogenesis, 26 metastasis, 28 and induction of apoptosis or autophagy are involved in sinomenine-mediated anti-tumor activity.…”

Section: Discussionmentioning

confidence: 99%

<p>Sinomenine Inhibits Non-Small Cell Lung Cancer via Downregulation of Hexokinases II-Mediated Aerobic Glycolysis</p>

Liu¹,

Yu²,

Zhou³

et al. 2020

OTT

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These authors contributed equally to this workBackground: Addiction to aerobic glycolysis is a common metabolic phenotype in human non-small cell lung cancer (NSCLC). The natural product Sinomenine (Sin) exhibits significant anti-tumor effects in various human cancers. However, the underlying mechanism remains elusive. Methods: The inhibitory effect of Sin on NSCLC cells was determined by MTS and soft agar assays. The glycolysis efficacy of NSCLC cells was examined by glucose uptake and lactate production. The activation of Akt signaling and the protein level of hexokinases II (HK2) were examined by immunoblot (IB), qRT-PCR, and immunohistochemical staining (IHC). The in vivo anti-tumor effect of Sin was validated by the xenograft mouse model. Results: We showed that HK2 is highly expressed in NSCLC tissues and cell lines. Depletion of HK2 suppressed cell viability, anchorage-independent colony formation, and xenograft tumor growth. Sinomenine exhibited a profound inhibitory effect on NSCLC cells by reducing HK2-mediated glycolysis both in vitro and in vivo. Ectopic overexpression of HK2 compromised these anti-tumor efficacies in sinomenine-treated NSCLC cells. Moreover, we revealed that sinomenine decreased Akt activity, which caused the downregulation of HK2-mediated glycolysis. Knockdown of Akt reduced HK2 protein level and impaired glycolysis. In contrast, overexpression of constitutively activated Akt1 reversed this phenotype. Conclusion: This study suggests that targeting HK2-mediated aerobic glycolysis is required for sinomenine-mediated anti-tumor activity.

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Retracted: Sinomenine exerts antitumour effect in gastric cancer cells via enhancement of miR‐204 expression

Cited by 16 publications

References 35 publications

Sinomenine Can Inhibit the Growth and Invasion Ability of Retinoblastoma Cell through Regulating PI3K/AKT Signaling Pathway

Sinomenine Can Inhibit the Growth and Invasion Ability of Retinoblastoma Cell through Regulating PI3K/AKT Signaling Pathway

The role of TRPV1 ion channels in the suppression of gastric cancer development

<p>Sinomenine Inhibits Non-Small Cell Lung Cancer via Downregulation of Hexokinases II-Mediated Aerobic Glycolysis</p>

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