Diosgenin inhibits Wnt/β-catenin pathway to regulate the proliferation and differentiation of MG-63 cells

Ge, Yunlin; Ding, Shuchen; Feng, Jianying; Du, Jinmei; Gu, Zenghui

doi:10.1007/s10616-021-00454-7

Cited by 9 publications

(7 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The anti-cancer effect of betanin against few cancer cell lines was previously reported [16][17][18][19] and the mechanism of actions was investigated. Earlier studies 20,21 showed that betanin altered ROS status, inhibited the peroxidation in lipid protein membrane and low-density lipoprotein, and stimulated the production of antioxidant secretions.…”

Section: Discussionmentioning

confidence: 99%

Betanin inhibits PI3K/AKT/mTOR/S6 signaling pathway, cell growth and death in osteosarcoma MG‐63 cells

Liu

Velu

Zheng³

et al. 2023

Environmental Toxicology

View full text Add to dashboard Cite

It is possible to develop new chemopreventive compounds so that cancer cells can be targeted in an exclusive manner. Bioactive natural compounds have demonstrated to be efficient chemotherapeutic agents, safe and cost‐effective. Majority of anti‐cancer medications are derived from natural sources, particularly of plant origins. Betanin (betanidin‐5‐O‐β‐glucoside) is the most common betacyanin with antioxidant, anti inflammatory and anticancer properties. The present study therefore investigated the effect of betanin onosteosarcoma MG‐63 cells. The mechanistic pathway of inflammatory responses, cell proliferation and apoptosis were investigated. The MG‐63 cells were treated with betanin for 24 h. Betanin actions on the appearance of cell arrangements, morphological changes, ROS induced Δψm, cell migration, cell adhesion and proliferative mechanistic marker expression of PI3K/AKT/mTOR/S6were analyzed. Betanin inhibited MG‐63 cells at IC50 concentrations between 9.08 and 54.49 μM and induced apoptosis by triggering the ROS mechanism. Betanin inhibited proliferation and migration of MG‐63 cells and induced DNA fragmentation. Betanin also modified the key mediator expression levels of PI3K/AKT/mTOR/S6 signaling pathways. Betanin can potentially be utilized in bone carcinoma therapeutics to inhibit, reverse or delay osteosarcoma.

show abstract

Section: Discussionmentioning

confidence: 99%

Betanin inhibits PI3K/AKT/mTOR/S6 signaling pathway, cell growth and death in osteosarcoma MG‐63 cells

Liu

Velu

Zheng³

et al. 2023

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…It was reported that transforming growth factor-β (TGF-β) and Wnt signaling was correlated with MESP1 in cardiomyocytes. 40 Particularly, diosgenin could also modulate TGF-β and Wnt signaling in various cell types, [41][42][43] leading to the concern that diosgenin may regulate MESP1 expression via modulating TGF-β and Wnt signaling.…”

Section: Discussionmentioning

confidence: 99%

Diosgenin inhibits the proliferation of gastric cancer cells via inducing mesoderm posterior 1 down-regulation-mediated alternative reading frame expression

Zheng

Zhao

et al. 2021

Hum Exp Toxicol

View full text Add to dashboard Cite

Introduction Whether and how mesoderm posterior 1 (MESP1) plays a role in the proliferation of gastric cancer cells remain unclear. Methods The expression of MESP1 was compared in 48 human gastric cancer tissues and adjacent normal tissues. Knockdown of MESP1 was performed to investigate the role of MESP1 in the proliferation and apoptosis of BGC-823 and MGC-803 gastric cancer cells. Knockdown of alternative reading frame (ARF) was performed to study the role of ARF in the inhibitory effect of MESP1 knockdown on cell proliferation in gastric cancer cells. Mouse subcutaneous xenograft tumor model bearing BGC-823 cells was used to investigate the role of MESP1 in the growth of gastric tumor in vivo. The effect of seven active ingredients from T. terrestris on MESP1 expression was tested. The anti-cancer effect of diosgenin was confirmed in gastric cancer cells. MESP1 dependence of the anti-cancer effect of diosgenin was confirmed by MESP1 knockdown. Results MESP1 was highly expressed in human gastric cancer tissues ( p < 0.05). MESP1 knockdown induced apoptosis and up-regulated the expression of ARF in gastric cancer cells ( p < 0.05). Knockdown of ARF attenuated the anti-cancer effect of MESP1 knockdown ( p < 0.05). In addition, MESP1 knockdown also suppressed tumor growth in vivo ( p < 0.05). Diosgenin inhibits both mRNA and protein expression of MESP1 ( p < 0.05). MESP1 knockdown attenuated the anti-cancer effect of diosgenin ( p < 0.05). Conclusions MESP1 promotes the proliferation of gastric cancer cells via inhibiting ARF expression. Diosgenin exerts anti-cancer effect through inhibiting MESP1 expression in gastric cancer cells.

show abstract

“…Human OS samples show a high association between the expression of WNT7B/WNT9A, LOXL2, and c‐FOS, and coexpression with c‐FOS/LOXL2 was linked to OS aggressiveness and shortened patient survival duration 85 . Syndcan2 (SDC2), a modulator of antitumor effects, inhibits SDC2 expression in the Wnt/β‐catenin pathway in OS cells, and reversal of the regulation increases SDC2 expression by secreting SFRP1, a Wnt signaling pathway antagonist, which improves OS disease progression 86 . Secretory Fzd‐related protein 2 (sFRP2) shows high expression in patients with OS and negatively correlates with patient survival.…”

Section: Signaling Pathways In Osmentioning

confidence: 99%

Targeting signaling pathways in osteosarcoma: Mechanisms and clinical studies

Shen

Lan

et al. 2023

MedComm

View full text Add to dashboard Cite

Osteosarcoma (OS) is a highly prevalent bone malignancy among adolescents, accounting for 40% of all primary malignant bone tumors. Neoadjuvant chemotherapy combined with limb‐preserving surgery has effectively reduced patient disability and mortality, but pulmonary metastases and OS cells' resistance to chemotherapeutic agents are pressing challenges in the clinical management of OS. There has been an urgent need to identify new biomarkers for OS to develop specific targeted therapies. Recently, the continued advancements in genomic analysis have contributed to the identification of clinically significant molecular biomarkers for diagnosing OS, acting as therapeutic targets, and predicting prognosis. Additionally, the contemporary molecular classifications have revealed that the signaling pathways, including Wnt/β‐catenin, PI3K/AKT/mTOR, JAK/STAT3, Hippo, Notch, PD‐1/PD‐L1, MAPK, and NF‐κB, have an integral role in OS onset, progression, metastasis, and treatment response. These molecular classifications and biological markers have created new avenues for more accurate OS diagnosis and relevant treatment. We herein present a review of the recent findings for the modulatory role of signaling pathways as possible biological markers and treatment targets for OS. This review also discusses current OS therapeutic approaches, including signaling pathway‐based therapies developed over the past decade. Additionally, the review covers the signaling targets involved in the curative effects of traditional Chinese medicines in the context of expression regulation of relevant genes and proteins through the signaling pathways to inhibit OS cell growth. These findings are expected to provide directions for integrating genomic, molecular, and clinical profiles to enhance OS diagnosis and treatment.

show abstract

Diosgenin inhibits Wnt/β-catenin pathway to regulate the proliferation and differentiation of MG-63 cells

Cited by 9 publications

References 34 publications

Betanin inhibits PI3K/AKT/mTOR/S6 signaling pathway, cell growth and death in osteosarcoma MG‐63 cells

Betanin inhibits PI3K/AKT/mTOR/S6 signaling pathway, cell growth and death in osteosarcoma MG‐63 cells

Diosgenin inhibits the proliferation of gastric cancer cells via inducing mesoderm posterior 1 down-regulation-mediated alternative reading frame expression

Targeting signaling pathways in osteosarcoma: Mechanisms and clinical studies

Contact Info

Product

Resources

About