The Role of Fallopia baldschuanica Plant Extract in the Regression of Induced Hepatocellular Carcinoma in Rats DOI Creative Commons

Luma Abd Almunim Baker,

Shaymaa Zuhir Jalal Aldin,

Hamza Hameed

et al.

Acta chimica slovenica, Journal Year: 2023, Volume and Issue: 70(4), P. 651 - 660

Published: Dec. 15, 2023

In 2020, around 19.3 million new cancer cases resulted in 3.5 deaths. It is estimated that there will be 28.4 by 2040. Plant-derived natural products, such as alkaloids, flavonoids, terpenoids, and phenolic compounds, offer a wide range of chemical structures biological activities can explored for their potential research. particular study, researchers investigated the anticancer effects Fallopia flower extracts on induced TAA (a carcinogen). They examined to identify specific amino acids with antioxidant properties assessed impact liver function tissue structure. The results showed plant had positive histological section TAA-treated group. Additionally, group male rats treated chemotherapy drug called MMC displayed effects. Similarly, TAA, extract, also These findings suggest extract from flowers could considered traditional therapy properties.

Language: Английский

Treating liver cancer through arginine depletion DOI
Yenisetti Rajendra Prasad,

J. Anakha,

Abhay H. Pande

et al.

Drug Discovery Today, Journal Year: 2024, Volume and Issue: 29(4), P. 103940 - 103940

Published: March 6, 2024

Language: Английский

Citations

10
Cellular Adaptation Takes Advantage of Atavistic Regression Programs during Carcinogenesis DOI Open Access
Davide Gnocchi, Dragana Nikolić,

Rosa Rita Paparella

et al.

Cancers, Journal Year: 2023, Volume and Issue: 15(15), P. 3942 - 3942

Published: Aug. 3, 2023

Adaptation of cancer cells to extreme microenvironmental conditions (i.e., hypoxia, high acidity, and reduced nutrient availability) contributes resilience. Furthermore, neoplastic transformation can be envisioned as an adaptive response tissue damage or chronic injury. The recent Systemic–Evolutionary Theory the Origin Cancer (SETOC) hypothesizes that “revert” “primitive” characteristics either ontogenically (embryo-like) phylogenetically (single-celled organisms). This regression may confer robustness maintain disordered state tissue, which is a hallmark malignancy. Changes in cell metabolism during adaptation also consequence altered conditions, often resulting shift toward lactic acid fermentation. However, mechanisms underlying robust capacity remain largely unknown. In years, cells’ metabolic flexibility has received increasing attention among researchers. Here, we focus on how changes microenvironment affect energy production drug sensitivity. Indeed, cellular lead “shift” “atavistic” biologic features, such switch from oxidative phosphorylation (OXPHOS) fermentation, sustain resistance. Finally, point out new integrative metabolism-based pharmacological approaches potential biomarkers for early detection.

Language: Английский

Citations

14
The Emerging Roles of the Metabolic Regulator G6PD in Human Cancers DOI Open Access

Alfar Ahamed,

Rendy Hosea, Shourong Wu

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(24), P. 17238 - 17238

Published: Dec. 7, 2023

Metabolic reprogramming, especially reprogrammed glucose metabolism, is a well-known cancer hallmark related to various characteristics of tumor cells, including proliferation, survival, metastasis, and drug resistance. Glucose-6-phosphate dehydrogenase (G6PD) the first rate-limiting enzyme pentose phosphate pathway (PPP), branch glycolysis, that converts glucose-6-phosphate (G6P) into 6-phosphogluconolactone (6PGL). Furthermore, PPP produces ribose-5-phosphate (R5P), which provides sugar-phosphate backbones for nucleotide synthesis as well nicotinamide adenine dinucleotide (NADPH), an important cellular reductant. Several studies have shown enhanced G6PD expression flux in their correlation with progression through regulation, reprogramming sustaining proliferative signaling, resisting cell death, activating invasion metastasis. Inhibiting could suppress promote reverse chemoresistance, inhibit suggesting potential target anti-tumor therapeutic strategies. Indeed, while challenges-including side effects-still remain, small-molecule inhibitors showing effect either when used alone or combination other drugs been developed. This review overview structural significance G6PD, its role regulation development progression, strategies explored relation G6PD-targeted therapy.

Language: Английский

Citations

11
Inhibition of PTPRE suppresses tumor progression and improves sorafenib response in hepatocellular carcinoma DOI Creative Commons
Renshun Dong, Tianci Wang, Wei Dong

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 173, P. 116366 - 116366

Published: March 8, 2024

Hepatocellular carcinoma (HCC) has a poor prognosis, and the efficacy of current therapeutic strategies is extremely limited in advanced diseases. Our previous study reported that protein tyrosine phosphatase receptor epsilon (PTPRE) promoting factor HCC progression. In this study, our objective was to evaluate treatment effect PTPRE inhibitors different preclinical models. results indicated inhibitory compound 63 (Cpd-63) inhibited tumor cell proliferation, migration, organoid growth. Mechanism research revealed Cpd-63 could inhibit expression MYC targets by inhibiting activation SRC. Additionally, we found improve response sorafenib cells. conclusion, demonstrated represented potential agent for management.

Language: Английский

Citations

4
The multifaceted roles of macrophages in the transition from hepatitis to hepatocellular carcinoma: From mechanisms to therapeutic strategies DOI
Shuairan Zhang, Dong Hang,

Xiuli Jin

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2025, Volume and Issue: 1871(3), P. 167676 - 167676

Published: Jan. 18, 2025

Language: Английский

Citations

0
DLAT is involved in ovarian cancer progression by modulating lipid metabolism through the JAK2/STAT5A/SREBP1 signaling pathway DOI Creative Commons

Hui Wang,

Shen Luo, Yue Yin

et al.

Cancer Cell International, Journal Year: 2025, Volume and Issue: 25(1)

Published: Jan. 27, 2025

Language: Английский

Citations

0
Role of hepatotropic viruses in promoting hepatocellular carcinoma—current knowledge and recent advances DOI

Piotr Starnawski,

Klaudia Nowak,

Zuzanna Augustyn

et al.

Medical Oncology, Journal Year: 2025, Volume and Issue: 42(4)

Published: March 17, 2025

Language: Английский

Citations

0
Lipids, cholesterols, statins and liver cancer: a Mendelian randomization study DOI Creative Commons

Zicheng Liang,

Zhen Zhang,

Xiaoning Tan

et al.

Frontiers in Oncology, Journal Year: 2023, Volume and Issue: 13

Published: Sept. 6, 2023

To investigate the causal relationship of serum lipid indicators and lipid-lowering drugs with risk liver cancer using Mendelian randomization study.A two-sample (TSMR) study was performed to between levels cancer, including low-density lipoprotein cholesterol (LDL-c), high-density (HDL-c), triglycerides (TG), total (TC), Apolipoprotein B (ApoB), A1 (ApoA1).Furthermore, instrumental variable weighted regression (IVW) summary data-based MR (SMR) analyses were effects drugs, statins PCSK9 inhibitors, on cancer.Serum LDL-c TC showed negatively associated (n = 22 SNPs, OR 0.363, 95% CI 0.231 - 0.570; p 1.070E-5) 83 SNPs; 0.627, 0.413-0.952; 0.028). However, TG, HDL-c, ApoA1 did not show any significant correlation cancer. In drug target (DMR) analyses, HMGCR-mediated level an inverse in IVW-MR analysis 5 0.201, 0.064 0.631; 5.95E-03) SMR 20 0.245, 0.065 0.926; 0.038) association based both analyses.Our results demonstrated that reduced increased Furthermore, targeting HMGCR such as

Language: Английский

Citations

10
IGF2BP2 promotes glycolysis and hepatocellular carcinoma stemness by stabilizing CDC45 mRNA via m6A modification DOI
Tao Wu, Li Liao, Tao Wu

et al.

Cell Cycle, Journal Year: 2023, Volume and Issue: 22(20), P. 2245 - 2263

Published: Oct. 18, 2023

A growing number of studies have shown the prognostic importance Cell division cycle protein 45 (CDC45) in hepatocellular carcinoma (HCC). This study aims to investigate biological function and mechanism CDC45 HCC. The differential expression significance HCC normal tissues were analyzed by bioinformatics. was knocked down effects vitro vivo measured. Subsequently, using RNA m6A colorimetry Methylated Immunoprecipitation (MeRIP), levels modification total evaluated cells. RIP applied establish that insulin-like growth factor 2 mRNA-binding (IGF2BP2) interact. test actinomycin D performed gauge stability mRNA. Furthermore, regulatory role IGF2BP2 on progression explored overexpressing IGF2BP2. High correlated with poor prognosis patients. Knocking inhibited cell proliferation, migration, invasion, EMT, stemness, glycolysis, promoted apoptosis, which verified through experiments. Additionally, highly expressed cells, it found interact CDC45. resulted reduced Moreover, overexpression while inhibiting reversed knocking In general, glycolysis stemness stabilizing mRNA via modification. KEYWORDS: HCCIGF2BP2CDC45 AcknowledgementsThe work supported funds from Hainan Provincial Key Laboratory Tumorigenesis Intervention, Open Project Fund (JCKF2021006). graphic abstract drawn Figdraw (www.figdraw.com).Disclosure statementNo potential conflict interest reported author(s).Supplementary materialSupplemental data for this article can be accessed online at https://doi.org/10.1080/15384101.2023.2283328.Additional informationFundingThe [JCKF2021006].

Language: Английский

Citations

9
β-HB treatment reverses sorafenib resistance by shifting glycolysis–lactate metabolism in HCC DOI Open Access
Fat‐Moon Suk,

Chien-Ying Wu,

Cheng-Chieh Fang

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 166, P. 115293 - 115293

Published: Aug. 9, 2023

Hepatocellular carcinoma (HCC) is the most common primary malignant tumor. Although sorafenib and regorafenib have been approved for first-line second-line treatment, respectively, of patients with advanced HCC, long-term treatment often results in acquired resistance. Given that glycolysis-mediated lactate production can contribute to drug resistance impair HCC efficacy, we investigated effects ketone body on metabolic shift sorafenib-resistant cells. We discovered differential expression 3-hydroxymethyl glutaryl-CoA synthase 2 (HMGCS2) D-β-hydroxybutyrate (β-HB) four cell lines. In cells, lower HMGCS2 β-HB levels were correlated more glycolytic alterations higher production. enhanced pyruvate dehydrogenase (PDH) decreased (LDHA) Additionally, combined or promoted antiproliferative antimigratory abilities cells by inhibiting B-raf/mitogen-activated protein kinase pathway mesenchymal N-cadherin-vimentin axis. vivo administration did not affect tumor growth, proliferative proteins was inhibited subcutaneous tumors. conclusion, exogenous reduce reverse inducing a shift; it also synergize treating HCC.

Language: Английский

Citations

8