Effects of Artonin E on Cell Growth Inhibition and Apoptosis Induction in Colon Cancer LoVo and HCT116 Cells

Abstract

Today, colon cancer is the leading cause of cancer death. In Thailand, colon cancer is the third most common cancer in men and the second in women. Currently, the treatments for colon cancer include surgery, chemotherapy, radiation therapy, immunotherapy, hormone therapy, targeted drug therapy, and stem cell therapy. However, some treatments have side effects for cancer patients, causing unwanted symptoms. In addition, targeted therapy comes with a high cost for patients. Therefore, bioactive compounds might be a good choice for colon cancer treatment. In this study, we investigated the effect of artonin E on apoptosis induction in colon cancer LoVo and HCT116 cells. The concentration ranges of artonin E at 3, 5, 10, and 30 µg/mL in LoVo cells and 1, 1.5, 2, and 3 µg/mL in HCT116 cells were examined. The results implied that artonin E decreased cell viability and increased apoptotic cells in a dose-dependent manner. In addition, artonin E stimulated mitochondrial membrane potential (ΔΨm) changes associated with apoptosis by increasing the sub-G1 population analyzed by flow cytometry. Western blotting showed that artonin E increased the proapoptotic protein, Bax, and decreased anti-apoptotic proteins’ (Bcl-2 and Bcl-x) expression. Moreover, artonin E also increased cleaved caspase-7 and cleaved-PARP expression in both LoVo and HCT116 cells. Interestingly, artonin E induced apoptosis through p-ERK1/2, p-p38/p38, and p-c-Jun expression in both cells. Our results suggested that artonin E induced apoptosis via caspase activation associated with the MAPKs signaling pathway. Therefore, artonin E might be used as a potential anticancer drug for colon cancer in the future.

Natural Prenylflavones from the Stem Bark of Artocarpus altilis: Promising Anticancer Agents for Oral Squamous Cell Carcinoma Targeting the Akt/mTOR/STAT-3 Signaling Pathway

“…Initially detected in the bark of AA, this molecule has been widely explored for its varied pharmacological activities, encompassing antibacterial, anticancer, antiestrogenic, anti-FAT10, antimalarial, antinephritis, antioxidant, and antiplasmodial activities . The anticancer effects of Artonin E have been explored across diverse cancer cell types, including breast (MCF-7, MDA-MB-231), , colon (LoVo, HCT116), , gastric cancers (AGS), leukemia (P-388), lung (H460, H23, H292, A549), , and ovarian (SKOV3, 1A9). , These studies highlight the potential of artonin E in inducing apoptosis, anoikis, and cell-cycle arrest and inhibiting proliferation, invasion, migration, and overcoming resistance to the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). – The underlying mechanisms involve activation and suppression of proapoptotic and antiapoptotic proteins, respectively.…”

Comprehensive Analysis of CLCA1 Expression, Immune Infiltration and Immune Checkpoints in Colon Adenocarcinoma

“…The exact cause of COAD remains uncertain, yet it is believed to have connection with various factors such as genetics, nutrition, inflammation, immunity, and microbiome (Birt & Phillips, 2014). Currently, surgery, radiation, and targeted medication therapy make up the majority of clinical management of COAD (Yangnok et al, 2022). However, certain individuals diagnosed with advanced colon adenocarcinoma (COAD) exhibit unresponsiveness towards radiation or chemotherapy treatment.…”

“…The study carried out by Nyström et al (2019), proposed that CLCA1 has a significant role in controlling the structural organization of mucus, thus contributing to the regulation of mucus processing. More importantly, it has been discovered in various research investigations that the expression of CLCA1 exhibits a strong association with the progression of cancer (Yang et al, 2013(Yang et al, , 2015. The expression of CLCA1 RNA and protein is low in malignant colon tissues (Praus et al, 2023).…”

Synthesis and Biological Evaluation of Some New 3-Aryl-2-thioxo-2,3-dihydroquinazolin-4(1H)-ones and 3-Aryl-2-(benzylthio)quinazolin-4(3H)-ones as Antioxidants; COX-2, LDHA, α-Glucosidase and α-Amylase Inhibitors; and Anti-Colon Carcinoma and Apoptosis-Inducing Agents

“…Conversely, during cancer development, the malignant cells alter this balance, by overexpressing various anti-apoptotic proteins and/or abnormally reduce the expression levels of pro-apoptotic members, and thus they become unresponsive to stimuli that otherwise trigger apoptosis in sensitive cells, which leads to cellular proliferation and cancer progression, in addition to therapeutic resistance [57]. Therefore, inhibiting the anti-apoptotic [58,59] and activating pro-apoptotic members [60] of the Bcl-2 family have been suggested as plausible selective strategies for cancer therapy and to overcome drug resistance.…”