INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2026
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IF 8.7
Qiyuan Luo,Shiqiang Li,Chenglong Zhang,Yijing Chen,Yun Chen
ALP1 is a structurally defined polysaccharide isolated from Amomum villosum T.L. Wu fruits with an average molecular weight of 26.1 kDa. Previous studies have demonstrated that ALP1 promotes growth performance of piglet by regulating proliferation of intestinal epithelial cells. However, the molecular mechanism remains incompletely understood. In the present study, the absorbability of ALP1 by porcine small intestine epithelial cells and regulating mechanism of ALP1 on cell proliferation were investigated. The results showed that ALP1 resists gastrointestinal degradation and is efficiently absorbed by intestinal epithelial cells via endocytosis. Furthermore, ALP1 facilitates cell cycle progression through upregulating expressions of cdk4 and cyclin e , resulting in an increased proportion of cells in the S and G2/M phases. These findings provide insights into the cellular mechanisms underlying the growth-promoting effects of ALP1 and highlight the potential of dietary polysaccharides as functional agents for enhancing animal growth and gut health.
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FOOD AND CHEMICAL TOXICOLOGY
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2026
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IF 3.2
Yang Yan,Yongfei Gu
Gastric cancer (GC) is a primary epithelial malignancy originating in the stomach. This research explored the influence and mechanism of Orientin on cellular senescence in GC. Orientin was predicted to regulate multiple cell cycle-related pathways, including cyclin-dependent protein kinase activity. Orientin docked with cyclin dependent kinase 2 (CDK2), cyclin A2 (CCNA2), cyclin E1 (CCNE1), and cyclin E2 (CCNE2) with binding energies of -9.1, -7.5, -7.2, and -8.3 kcal/mol, respectively. The IC 50 values of Orientin for AGS and HGC-27 cells were 24.33 μM and 39.28 μM, respectively. Orientin dose-dependently inhibited GC cell proliferation, promoted G0/G1 phase arrest, as well as downregulated CDK2, CCNA2, CCNE1, and CCNE2 expression. It enhanced senescence-associated β-galactosidase staining intensity, upregulated p16 and p21, and downregulated phosphorylated retinoblastoma (p-Rb). In vivo , Orientin also suppressed tumor progression, promoted p16 and p21 expression, and inhibited CCNE/CCNA-CDK2 signaling. Orientin exerts anti-cancer effects in GC through triggering cellular senescence and cell cycle arrest, likely via activating p16/p21-Rb signaling axis and inhibiting the CCNE/CCNA-CDK2 pathway. Download: Download high-res image (282KB) Download: Download full-size image
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3 Biotech
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2021
·Vol. 11
·期 8
·1-11
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IF 2.406
Wang Dekang,Hu Aili,Peng Hao,Li Dongbo,Zhang Li
Glioma is the most common primary brain tumor in adults with an adverse prognosis and obscure pathogenesis. PICALM interacting mitotic regulator protein (PIMREG) functions as an oncogene in multiple types of cancer, but its function in glioma remains unknown. The Gene Expression Profiling Interactive Analysis 2 (GEPIA2, http://gepia2.cancer-pku.cn/#index ) showed that PIMREG expression in the glioma tissues was higher than that in normal brain tissues. Herein, cell counting kit-8 assay and flow cytometry analysis exhibited that overexpression of PIMREG significantly promoted the proliferation of glioma cells and the transition from G1 phase of the cell cycle to S phase. Wound-healing and transwell assays showed that overexpression of PIMREG markedly enhanced the migration and invasion of glioma cells. Western blot analysis revealed that overexpression of PIMREG increased the expression of cyclin D1, cyclin E, Vimentin, matrix metalloproteinase (MMP)-2, and MMP-9, but reduced the expression of E-cadherin. In addition, overexpression of PIMREG activated the β-catenin signaling pathway, as evidenced by the increased total and nuclear expression of β-catenin and the up-regulated expression of its downstream target c-myc. Furthermore, immunofluorescence staining further indicated the increased nuclear translocation of β-catenin in PIMREG-overexpressing cells. However, knockdown of PIMREG exerted opposite effects on glioma cells. Blockade of the β-catenin signaling by ICG-001 markedly impeded the promoting effects of PIMREG on glioma cell proliferation and invasion. In conclusion, PIMREG acts as a tumor promoter in glioma at least partly via activating the β-catenin signaling pathway. This study provides new insights into the molecular mechanism for glioma pathogenesis and treatment.
研究领域:
肿瘤学
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神经科学
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细胞生物学
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分子生物学
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Reproductive Biology
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2018
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IF 1.446
Zhen Luo,Wenli Luo,Shaohua Li,Sen Zhao,Takami Sho,Xue Xu,Jing Zhang,Weina Xu,Jianxiong Xu
Intrauterine growth restriction (IUGR) remains a significant obstacle in pig production; however, information regarding the relationship between reactive oxygen species (ROS)-induced placental dysfunction and IUGR is still unknown. This study aimed to explore the placental redox status, mitochondrial content, cellular progression, and mitogen-activated protein kinase (MAPK) pathways in IUGR. Placental tissues were collected from normal intrauterine gestation (NIUG) and IUGR fetuses at delivery. Compared with the NIUG, placental ROS production, lipid peroxidation , and DNA damage were increased in IUGR. Placental mitochondrial DNA (mtDNA) content and mtDNA-encoded gene expression decreased in IUGR. Moreover, p21 phosphorylation increased, cyclin E expression decreased in IUGR cases, which showed senescence characteristics. Analysis of signaling pathways showed that the ERK1/2 phosphorylation increased whereas the p38 and JNK phosphorylation decreased in IUGR. In cultured porcine trophectoderm (pTr) cells, exogenous H 2 O 2 increased intracellular ROS production, decreased cell viability in a dose-dependent manner. Cell cycle distribution was found to arrest in S and G2/M phases. Our findings suggested that IUGR was associated with greater placental ROS and oxidative injury, which might be a factor that resulted in lower mitochondrial content, microvilli loss and senescence, and activation of MAPK pathways.
研究领域:
动物科学
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生殖生物学
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分子生物学
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细胞生物学
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