scholarly journals Glycosidic flavonoids and their potential applications in cancer research: a review

Author(s):  
Abuyaseer Abusaliya ◽  
Sang Eun Ha ◽  
Pritam Bhagwan Bhosale ◽  
Hun Hwan Kim ◽  
Min Yeong Park ◽  
...  

Abstract Purpose of review Every year, the cancer patient registry increases, and the leading cause of death in a global context. Plant-based molecules are gaining attention in cancer research due to the side effects of chemotherapy. A glycosidic derivative of flavonoid (GDF) plays a significant role in cancer proliferation mechanisms. GDF inhibits cell proliferation by elevating the expression of apoptotic proteins, altering the expression of nuclear factor-kappa B (NF- κB), and decreasing mitochondrial membrane potential (Δψm) in cancer cells. Recent findings Reported studies on the flavonoids orientin, vitexin, prunetionoside, chrysin, and scutellarein increased attention and are being widely investigated for their potential role in different parts of cancer research. Prunetionoside is a flavonoid with high cytotoxic potential and capable of inducing necroptosis in AGS gastric cancer cells. Similarly, scutellarein is a flavonol, induces an extrinsic apoptotic pathway and downregulates the expression level of cyclin proteins in HepG2 liver cancer cells. Vitexin is reported to be capable of deregulating the expression levels of p-Akt, p-mTOR, and p-PI3K in A549 lung cancer cells. Orientin inhibits IL-8 expression and invasion in MCF-7 breast cancer cells by suppressing MMP-9 in the presence of TPA via STAT3/AP-1/ERK/PKCα-mediated signaling pathways. It also induces mitochondria-mediated intrinsic apoptosis and G0/G1 cell cycle arrest in HT29 colon cancer cells. Chrysin is a flavonoid present in honey that has been shown to play an important role in cervical and colon cancer by suppressing the AKT/mTOR/PI3K pathway and increasing ROS accumulation, LDH leakage, respectively.

2017 ◽  
Vol 33 ◽  
pp. 112-121 ◽  
Author(s):  
Fatima Zahra Ghanemi ◽  
Meriem Belarbi ◽  
Aurélie Fluckiger ◽  
Abdelhafid Nani ◽  
Adélie Dumont ◽  
...  

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4417
Author(s):  
Rabin Neupane ◽  
Saloni Malla ◽  
Mariam Sami Abou-Dahech ◽  
Swapnaa Balaji ◽  
Shikha Kumari ◽  
...  

A novel series of 4-anilinoquinazoline analogues, DW (1–10), were evaluated for anticancer efficacy in human breast cancer (BT-20) and human colorectal cancer (CRC) cell lines (HCT116, HT29, and SW620). The compound, DW-8, had the highest anticancer efficacy and selectivity in the colorectal cancer cell lines, HCT116, HT29, and SW620, with IC50 values of 8.50 ± 2.53 µM, 5.80 ± 0.92 µM, and 6.15 ± 0.37 µM, respectively, compared to the non-cancerous colon cell line, CRL1459, with an IC50 of 14.05 ± 0.37 µM. The selectivity index of DW-8 was >2-fold in colon cancer cells incubated with vehicle. We further determined the mechanisms of cell death induced by DW-8 in SW620 CRC cancer cells. DW-8 (10 and 30 µM) induced apoptosis by (1) producing cell cycle arrest at the G2 phase; (2) activating the intrinsic apoptotic pathway, as indicated by the activation of caspase-9 and the executioner caspases-3 and 7; (3) nuclear fragmentation and (4) increasing the levels of reactive oxygen species (ROS). Overall, our results suggest that DW-8 may represent a suitable lead for developing novel compounds to treat CRC.


Author(s):  
Kon-Young Ji ◽  
Ki Mo Kim ◽  
Yun Hee Kim ◽  
Ki-Shuk Shim ◽  
Joo Young Lee ◽  
...  

The molecular mechanism underlying the anticancer effects of Anemarrhena asphodeloides (A. asphodeloides) on colon cancer is unknown. This is the first study evaluating the anticancer effect of A. asphodeloides extract (AA-Ex) in serum-starved colorectal cancer cells. Changes in cell proliferation and morphology in serum-starved MC38 and HCT116 colorectal cancer cells were investigated using MTS assay. Cell cycle and apoptosis were investigated using flow cytometry, and cell cycle regulator expression was determined using qRT-PCR. Apoptosis regulator protein levels and mitogen-activated protein kinase (MAPK) phosphorylation were assessed using western blotting. AA-Ex sensitively suppressed proliferation of serum-starved colorectal cancer cells, with MC38 and HCT116 cells showing greater changes in proliferation after treatment with AA-Ex under serum starvation than HaCaT and RAW 264.7 cells. AA-Ex inhibited cell cycle progression in serum-starved MC38 and HCT116 cells and increased the expression of cell cycle inhibitors (p53, p21, and p27). Furthermore, AA-Ex induced apoptosis in serum-starved MC38 and HCT116 cells. Consistently, AA-Ex suppressed the expression of the anti-apoptotic molecule Bcl-2 and upregulated pro-apoptotic molecules (cytochrome c, cleaved caspase-9, cleaved caspase-3, and cleaved-PARP) in serum-starved cells. AA-Ex treatment under serum starvation decreased AKT and ERK1/2 phosphorylation in the cell survival signaling pathway but increased p38 and JNK phosphorylation. Furthermore, AA-Ex treatment with serum starvation increased the levels of the transcription factors of the p38 and JNK pathway. Serum starvation sensitizes colorectal cancer cells to the anticancer effect of A. asphodeloidesvia p38/JNK-induced cell cycle arrest and apoptosis. Hence, AA-Ex possesses therapeutic potential for colon cancer treatment.


Sign in / Sign up

Export Citation Format

Share Document