Bisdemethoxycurcumin promotes apoptosis in human platelets via activation of ERK signaling pathway

Paul, Manoj; Manikanta, Kurnegala; Hemshekhar, Mahadevappa; Sundaram, Mahalingam S.; Naveen, S.; Ramesh, T. N.; Kemparaju, K.; Girish, K. S.

doi:10.1016/j.tiv.2019.104743

Cited by 11 publications

(5 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results of the mRNA changes in p21 and MYC confirmed that the MAPK pathway was activated. Although the majority of studies have demonstrated that the p-p44/42 MAPK pathway exerts an anti-apoptotic role, p-p44/42 MAPK signaling has also been demonstrated to exhibit a pro-apoptotic effect, such as in neurons ( 35 ), platelets ( 36 ) and cardiomyocytes ( 37 ). Studies have demonstrated that overactivation of MAPK and TGF-β signaling pathways in low-risk MDS can promote excessive apoptosis of hematopoietic stem cells, whereas the AKT/PI3K, PI3K/mTOR and EGF signaling pathways are overactivated in high-risk MDS ( 38 – 41 ).…”

Section: Discussionmentioning

confidence: 99%

IGF‑IR promotes clonal cell proliferation in myelodysplastic syndromes via inhibition of the MAPK pathway

Zheng

et al. 2020

Oncol Rep

View full text Add to dashboard Cite

Type 1 insulin-like growth factor receptor (IGF-IR) signaling is considered to serve a key role in the development of cancer. However, the effects of IGF-IR on the malignant characteristics of myelodysplastic syndrome (MDS) clonal cells remains to be determined. In the present study it was demonstrated that knockdown of IGF-IR reduced the proliferation and increased the apoptosis of MDS/leukemia cells. Integrated analysis of gene expression profiles using bioinformatics identified the MAPK signaling pathway as a critical downstream factor of IGF-IR, and this was confirmed in vitro using western blotting which revealed that IGF-IR knockdown significantly increased the expression of activated MAPK. Furthermore, IGF-IR signaling was inhibited to investigate the potential of IGF-IR as a therapeutic target of MDS. The results revealed that the IGF-IR inhibitor picropodophyllin (PPP) inhibited cell proliferation, promoted cell apoptosis and arrested the cell cycle at the G2/M phase in MDS/leukemia cells. Similar to the effects of IGF-IR knockdown, PPP treatment also increased MAPK signaling in vitro. In conclusion, IGF-IR may serve as a potential therapeutic target of MDS.

show abstract

Section: Discussionmentioning

confidence: 99%

IGF‑IR promotes clonal cell proliferation in myelodysplastic syndromes via inhibition of the MAPK pathway

Zheng

et al. 2020

Oncol Rep

View full text Add to dashboard Cite

show abstract

“…Bisdemethoxycurcumin is a demethoxy derivative of curcumin and is much more stable than curcumin in physiological media [ 514 , 515 , 516 ]. It can scavenge free radicals and control cellular redox balance because of its antioxidant property [ 517 , 518 ], and it has potential anti-allergic effects [ 519 ].…”

Section: The Health Benefits Of Curcuminoids (Curcumin Demethoxycurcu...mentioning

confidence: 99%

Therapeutic Potential of Phenolic Compounds in Medicinal Plants—Natural Health Products for Human Health

2023

View full text Add to dashboard Cite

Phenolic compounds and flavonoids are potential substitutes for bioactive agents in pharmaceutical and medicinal sections to promote human health and prevent and cure different diseases. The most common flavonoids found in nature are anthocyanins, flavones, flavanones, flavonols, flavanonols, isoflavones, and other sub-classes. The impacts of plant flavonoids and other phenolics on human health promoting and diseases curing and preventing are antioxidant effects, antibacterial impacts, cardioprotective effects, anticancer impacts, immune system promoting, anti-inflammatory effects, and skin protective effects from UV radiation. This work aims to provide an overview of phenolic compounds and flavonoids as potential and important sources of pharmaceutical and medical application according to recently published studies, as well as some interesting directions for future research. The keyword searches for flavonoids, phenolics, isoflavones, tannins, coumarins, lignans, quinones, xanthones, curcuminoids, stilbenes, cucurmin, phenylethanoids, and secoiridoids medicinal plant were performed by using Web of Science, Scopus, Google scholar, and PubMed. Phenolic acids contain a carboxylic acid group in addition to the basic phenolic structure and are mainly divided into hydroxybenzoic and hydroxycinnamic acids. Hydroxybenzoic acids are based on a C6-C1 skeleton and are often found bound to small organic acids, glycosyl moieties, or cell structural components. Common hydroxybenzoic acids include gallic, syringic, protocatechuic, p-hydroxybenzoic, vanillic, gentistic, and salicylic acids. Hydroxycinnamic acids are based on a C6-C3 skeleton and are also often bound to other molecules such as quinic acid and glucose. The main hydroxycinnamic acids are caffeic, p-coumaric, ferulic, and sinapic acids.

show abstract

“…The curcuminoids in the turmeric acetone extract are crucial for the gastroprotective effect against ethanol-induced damage [ 14 ]. BDMC prevented kidney fibrosis by activating fibroblast apoptosis [ 15 ] and promoted apoptosis in human platelets via activation of ERK signaling pathway [ 16 ]. It induced cell apoptosis in liver cancer Hep 3B cells [ 17 ] and induced caspase-dependent and -independent apoptosis via Smad or Akt signaling pathways in osteosarcoma HOS cells [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Bisdemethoxycurcumin Induces Cell Apoptosis and Inhibits Human Brain Glioblastoma GBM 8401/Luc2 Cell Xenograft Tumor in Subcutaneous Nude Mice In Vivo

Hsia

Peng

Chueh

et al. 2022

IJMS

View full text Add to dashboard Cite

Bisdemethoxycurcumin (BDMC) has biological activities, including anticancer effects in vitro; however, its anticancer effects in human glioblastoma (GBM) cells have not been examined yet. This study aimed to evaluate the tumor inhibitory effect and molecular mechanism of BDMC on human GBM 8401/luc2 cells in vitro and in vivo. In vitro studies have shown that BDMC significantly reduced cell viability and induced cell apoptosis in GBM 8401/luc2 cells. Furthermore, BDMC induced apoptosis via inhibited Bcl-2 (anti-apoptotic protein) and increased Bax (pro-apoptotic proteins) and cytochrome c release in GBM 8401/luc2 cells in vitro. Then, twelve BALB/c-nude mice were xenografted with human glioblastoma GBM 8401/luc2 cancer cells subcutaneously, and the xenograft nude mice were treated without and with BDMC (30 and 60 mg/kg of BDMC treatment) every 3 days. GBM 8401/luc2 cell xenografts experiment showed that the growth of the tumors was significantly suppressed by BDMC administration at both doses based on the reduction of tumor size and weights. BDMC did not change the body weight and the H&E histopathology analysis of liver samples, indicating that BDMC did not induce systemic toxicity. Meanwhile, treatment with BDMC up-regulated the expressions of BAX and cleaved caspase-3, while it down-regulated the protein expressions of Bcl-2 and XIAP in the tumor tissues compared with the control group. This study has demonstrated that BDMC presents potent anticancer activity on the human glioblastoma GBM 8401/luc2 cell xenograft model by inducing apoptosis and inhibiting tumor cell proliferation and shows the potential for further development to the anti-GBM cancer drug.

show abstract

Bisdemethoxycurcumin promotes apoptosis in human platelets via activation of ERK signaling pathway

Cited by 11 publications

References 20 publications

IGF‑IR promotes clonal cell proliferation in myelodysplastic syndromes via inhibition of the MAPK pathway

IGF‑IR promotes clonal cell proliferation in myelodysplastic syndromes via inhibition of the MAPK pathway

Therapeutic Potential of Phenolic Compounds in Medicinal Plants—Natural Health Products for Human Health

Bisdemethoxycurcumin Induces Cell Apoptosis and Inhibits Human Brain Glioblastoma GBM 8401/Luc2 Cell Xenograft Tumor in Subcutaneous Nude Mice In Vivo

Contact Info

Product

Resources

About