Odontogenic ameloblast-associated protein (ODAM) inhibits human colorectal cancer growth by promoting PTEN elevation and inactivating PI3K/AKT signaling

Yu, Minhao; Mu, Yi-Fei; Yang, Qing; Qin, Shao-Lan; Qiu, Yier; Cui, Ran; Zhong, Ming

doi:10.1016/j.biopha.2016.09.076

Cited by 12 publications

(16 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PTEN is known to inhibit the activity of PI3K, which then affects the phosphorylation of Akt (12). The PI3K/PTEN/Akt signal pathway has been demonstrated to play a role in a variety of tumors including hematological neoplasms, liver cancer, intestinal cancer, osteosarcoma, and lymphoma (13)(14)(15)(16). This pathway was recently found to be closely related to chronic inflammatory diseases and autoimmune diseases such as asthma (17).…”

Section: Introductionmentioning

confidence: 99%

PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

2017

View full text Add to dashboard Cite

Chronic rhinosinusitis (CRS) is a form of chronic inflammation of the nasal cavity and paranasal sinus with multi‑causal pathogenesis, including oxidative stress. Several lines of evidence have demonstrated that the phosphatase and tensin homolog gene (PTEN) can inhibit the activation of phosphoinositide 3‑kinase (PI3K) to affect phosphorylation of Akt. Importantly, the PI3K/PTEN/Akt signaling pathway is associated with various types of tumors, chronic inflammatory diseases, and autoimmune disease through its regulation of cell growth, apoptosis, proliferation, and metabolism. This in vitro study aimed to investigate the role of PTEN and the relationship between PTEN and the PI3K/Akt pathway in nasal epithelial cells under oxidative stress. H2O2 treatment was applied to induce a cell injury model of oxidative stress in rat nasal epithelial cells. Cells were divided into control, H2O2, H2O2+PTEN, and H2O2+siPTEN groups. Cell viability was measured using the CCK‑8 assay, and reactive oxygen species (ROS) levels and apoptosis rates were analyzed by flow cytometry (FCM). Oxidative parameters, including ROS, catalase (CAT), and malondialdehyde (MDA), were tested by enzyme‑linked immunosorbent assay (ELISA). The expression of apoptosis‑related genes and PI3K/Akt pathway was assayed by quantitative PCR (qPCR) and western blot. In H2O2‑injured cells, oxidative stress, due to increased ROS levels and apoptosis rates, was induced, and PTEN aggravated the injury. The levels of both p‑Akt and PTEN in H2O2‑injured cells were positively correlated and higher than in control cells. Unknown regulatory protein(s) may exist in the PI3K/PTEN/Akt pathway or the PTEN and PI3K/Akt pathways may be two independent signaling pathways that have cross interactions.

show abstract

Section: Introductionmentioning

confidence: 99%

PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

2017

View full text Add to dashboard Cite

show abstract

“…Cells in the logarithmic phase were seeded into 96-well plates (approximately 5 × 10 4 cells/well) and maintained for 12 h in the incubator (37 °C, 5% CO 2 ). Next, EELs at different concentrations (5,10,25,50, 75 and 100 mg/ml) were incubated with the cells in the incubator (37 °C, 5% CO 2 ) for 48 h.…”

Section: Cell Counting Kit-8 (Cck-8) Assaymentioning

confidence: 99%

“…Effect of EEL on viability of Bel-7402 nd Huh-7 cells. After being treated with different concentrations of EEL (5,10,25,50,75, and 100 mg/ml), cell viability in each group was determined using CCK-8 assay at 12, 24 and 48 h. Data were shown as mean ± S.D for three independent experiments. * P < 0.05, ** P < 0.01 versus control.…”

Section: Supplementary Informationmentioning

confidence: 99%

“…4 TCM Gynecology, Hangzhou Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang Province, China. 5 Department of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang Province, China.…”

Section: Supplementary Informationmentioning

confidence: 99%

“…Molecular target therapy in cancer treatment has attracted much attention and it is also necessary to further understand the molecular mechanism of HCC progression. Previous researches showed that the PI3K/ PTEN/Akt pathway was closely involved in malignant tumors such as hepatocellular carcinoma, hematological neoplasms and lymphoma [4][5][6][7]. PI3K phosphorylates PIP2, and generates PIP3 which is then used by PDK1/ PDPK1 (3-phosphoinositide-dependent protein kinase 1) to phosphorylate AKT.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Ethanol extract of Ligustrum lucidum Ait. leaves suppressed hepatocellular carcinoma in vitro and in vivo

et al. 2019

View full text Add to dashboard Cite

Background: The present study investigated the pharmacological activity and mechanism of ethanol extract of Ligustrum lucidum Ait. leaves (EEL) on HCC. Methods: Cell viability was determined using cell counting kit-8 (CCK-8) assay. The effects of EEL on cellular biological activities were analyzed by flow cytometry (FCM), cell wound scratch assay and transwell assay. The expression levels of related mRNA and protein were determined by performing quantitative real-time PCR (qRT-PCR), Western blotting assay and immunocytochemistry. Methylation-specific PCR (MSP) was carried out to investigate the possible mechanism underlying the DNA methylation of PTEN. Results: EEL showed cytotoxicity to both Bel-7402 and Huh-7 cell lines. We also found that EEL enhanced the apoptosis of Bel-7402 and Huh-7 cells by regulating the expressions of Bcl-2 associated X (Bax), B cell lymphoma 2 (Bcl-2) and Cytochrome-C and the activity of caspase-3 and therefore promoted cell cycle arrest. Moreover, EEL also suppressed cell migration and invasion. EEL increased the expression of tissue inhibitor of metalloproteinases 2 (TIMP2) but decreased the expressions of matrix metalloproteinase2 (MMP2) and MMP9. Furthermore, EEL inhibited the phosphorylation of PI3K/Akt pathway. MSP results showed that EEL promoted the demethylation of PTEN, suggesting that the inactivation of PI3K/Akt may be related to DNA de-methylation of PTEN. In addition, EEL inhibited the tumor growth of HCC in vivo. Conclusions: EEL exerted anti-tumor effect on HCC in vitro and in vivo. EEL mediated by the inhibition of PI3K/Akt may be closely related to DNA de-methylation of PTEN. Thus, EEL could be used as a potential anti-cancer therapeutic agent of HCC.

show abstract

Downregulation of odontogenic ameloblast-associated protein in the progression of periodontal disease affects cell adhesion, proliferation, and migration

Hou

Liu

Yan

et al. 2023

Archives of Oral Biology

View full text Add to dashboard Cite

Odontogenic ameloblast-associated protein (ODAM) inhibits human colorectal cancer growth by promoting PTEN elevation and inactivating PI3K/AKT signaling

Cited by 12 publications

References 28 publications

PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

Ethanol extract of Ligustrum lucidum Ait. leaves suppressed hepatocellular carcinoma in vitro and in vivo

Downregulation of odontogenic ameloblast-associated protein in the progression of periodontal disease affects cell adhesion, proliferation, and migration

Contact Info

Product

Resources

About