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BioResource International Inc human cervical cancer cell lines caski
Human Cervical Cancer Cell Lines Caski, supplied by BioResource International Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human cervical cancer cell lines caski/product/BioResource International Inc
Average 90 stars, based on 1 article reviews
human cervical cancer cell lines caski - by Bioz Stars, 2026-03
90/100 stars

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PTEN silencing regulates the expression levels of proteins involved in apoptosis and the cell cycle. (A-C) Western blots showing the levels of proteins involved in apoptosis (caspase-3, MDM2, PARP, p21, p27, p53 and Bax), cell cycle (cyclin D1, cyclin A2, cyclin B1, cyclin E1 and CDK6), and AKT and ERK signaling pathways <t>in</t> <t>cervical</t> cancer cells transfected with PTEN siRNA1. (D) Cell viability of <t>HeLa</t> and CaSki cells transfected with PTEN-targeting and control siRNAs (error bars represent 95% confidence intervals). ** P<0.01 vs. control siRNA. siRNA, small interfering RNA; CTL, control siRNA; PTEN1, PTEN siRNA1.
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PTEN silencing regulates the expression levels of proteins involved in apoptosis and the cell cycle. (A-C) Western blots showing the levels of proteins involved in apoptosis (caspase-3, MDM2, PARP, p21, p27, p53 and Bax), cell cycle (cyclin D1, cyclin A2, cyclin B1, cyclin E1 and CDK6), and AKT and ERK signaling pathways <t>in</t> <t>cervical</t> cancer cells transfected with PTEN siRNA1. (D) Cell viability of <t>HeLa</t> and CaSki cells transfected with PTEN-targeting and control siRNAs (error bars represent 95% confidence intervals). ** P<0.01 vs. control siRNA. siRNA, small interfering RNA; CTL, control siRNA; PTEN1, PTEN siRNA1.
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Metformin inhibits cervical cancer cell proliferation and migration. (A) CaSki, <t>C33A</t> and HeLa cells were treated with metformin (0–20 mM) for 48 h. Cell viability was determined by performing the Cell Counting Kit-8 assay. (B) CaSki, C33A and HeLa cells were treated with metformin (0–10 mM) for 48 h. Cell migration was assessed by performing a Transwell migration assay (scale bar, 200 µm). Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin.
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PTEN silencing regulates the expression levels of proteins involved in apoptosis and the cell cycle. (A-C) Western blots showing the levels of proteins involved in apoptosis (caspase-3, MDM2, PARP, p21, p27, p53 and Bax), cell cycle (cyclin D1, cyclin A2, cyclin B1, cyclin E1 and CDK6), and AKT and ERK signaling pathways in cervical cancer cells transfected with PTEN siRNA1. (D) Cell viability of HeLa and CaSki cells transfected with PTEN-targeting and control siRNAs (error bars represent 95% confidence intervals). ** P<0.01 vs. control siRNA. siRNA, small interfering RNA; CTL, control siRNA; PTEN1, PTEN siRNA1.

Journal: Experimental and Therapeutic Medicine

Article Title: PTEN downregulation induces apoptosis and cell cycle arrest in uterine cervical cancer cells

doi: 10.3892/etm.2021.10534

Figure Lengend Snippet: PTEN silencing regulates the expression levels of proteins involved in apoptosis and the cell cycle. (A-C) Western blots showing the levels of proteins involved in apoptosis (caspase-3, MDM2, PARP, p21, p27, p53 and Bax), cell cycle (cyclin D1, cyclin A2, cyclin B1, cyclin E1 and CDK6), and AKT and ERK signaling pathways in cervical cancer cells transfected with PTEN siRNA1. (D) Cell viability of HeLa and CaSki cells transfected with PTEN-targeting and control siRNAs (error bars represent 95% confidence intervals). ** P<0.01 vs. control siRNA. siRNA, small interfering RNA; CTL, control siRNA; PTEN1, PTEN siRNA1.

Article Snippet: The human cervical cancer cell lines HeLa and CaSki (Korean Cell Line Bank) were used.

Techniques: Expressing, Western Blot, Protein-Protein interactions, Transfection, Control, Small Interfering RNA

Metformin inhibits cervical cancer cell proliferation and migration. (A) CaSki, C33A and HeLa cells were treated with metformin (0–20 mM) for 48 h. Cell viability was determined by performing the Cell Counting Kit-8 assay. (B) CaSki, C33A and HeLa cells were treated with metformin (0–10 mM) for 48 h. Cell migration was assessed by performing a Transwell migration assay (scale bar, 200 µm). Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin.

Journal: Molecular Medicine Reports

Article Title: Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells

doi: 10.3892/mmr.2020.11725

Figure Lengend Snippet: Metformin inhibits cervical cancer cell proliferation and migration. (A) CaSki, C33A and HeLa cells were treated with metformin (0–20 mM) for 48 h. Cell viability was determined by performing the Cell Counting Kit-8 assay. (B) CaSki, C33A and HeLa cells were treated with metformin (0–10 mM) for 48 h. Cell migration was assessed by performing a Transwell migration assay (scale bar, 200 µm). Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin.

Article Snippet: The CaSki, HeLa and C33A human cervical cancer cell lines were purchased from the Bioresource Collection and Research Center.

Techniques: Migration, Cell Counting, Transwell Migration Assay

Metformin induces cervical cancer cell apoptosis. CaSki, C33A and HeLa cells were treated with metformin (0, 5 or 10 mM) for 48 h. Cell apoptosis was (A) determined via flow cytometry and (B) quantified. Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin.

Journal: Molecular Medicine Reports

Article Title: Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells

doi: 10.3892/mmr.2020.11725

Figure Lengend Snippet: Metformin induces cervical cancer cell apoptosis. CaSki, C33A and HeLa cells were treated with metformin (0, 5 or 10 mM) for 48 h. Cell apoptosis was (A) determined via flow cytometry and (B) quantified. Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin.

Article Snippet: The CaSki, HeLa and C33A human cervical cancer cell lines were purchased from the Bioresource Collection and Research Center.

Techniques: Flow Cytometry

Metformin induces cervical cancer cell cycle arrest. CaSki, C33A and HeLa cells were treated with metformin (0, 5 or 10 mM) for 48 h. Cell cycle phase distribution was (A) determined via flow cytometry and (B) quantified. Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin.

Journal: Molecular Medicine Reports

Article Title: Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells

doi: 10.3892/mmr.2020.11725

Figure Lengend Snippet: Metformin induces cervical cancer cell cycle arrest. CaSki, C33A and HeLa cells were treated with metformin (0, 5 or 10 mM) for 48 h. Cell cycle phase distribution was (A) determined via flow cytometry and (B) quantified. Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin.

Article Snippet: The CaSki, HeLa and C33A human cervical cancer cell lines were purchased from the Bioresource Collection and Research Center.

Techniques: Flow Cytometry

Effect of metformin on AMPK and caspase-dependent apoptosis signaling in cervical cancer cell lines. CaSki, C33A and HeLa cells were treated with metformin (0, 5 or 10 mM) for 48 h. p-AMPK, AMPK, p-p53, p53, Bcl-2, Bak, Bax and cleaved caspase-3 protein expression levels were (A) determined via western blotting and semi-quantified in (B) CaSki, (C) C33A and (D) HeLa cells. Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. AMPK, AMP-activated protein kinase; p, phosphorylated; Bak, Bcl-2 antagonist/killer 1; CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin; C-cas-3, cleaved caspase-3.

Journal: Molecular Medicine Reports

Article Title: Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells

doi: 10.3892/mmr.2020.11725

Figure Lengend Snippet: Effect of metformin on AMPK and caspase-dependent apoptosis signaling in cervical cancer cell lines. CaSki, C33A and HeLa cells were treated with metformin (0, 5 or 10 mM) for 48 h. p-AMPK, AMPK, p-p53, p53, Bcl-2, Bak, Bax and cleaved caspase-3 protein expression levels were (A) determined via western blotting and semi-quantified in (B) CaSki, (C) C33A and (D) HeLa cells. Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. AMPK, AMP-activated protein kinase; p, phosphorylated; Bak, Bcl-2 antagonist/killer 1; CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin; C-cas-3, cleaved caspase-3.

Article Snippet: The CaSki, HeLa and C33A human cervical cancer cell lines were purchased from the Bioresource Collection and Research Center.

Techniques: Expressing, Western Blot

Effects of metformin on PI3K/AKT/mTOR signaling in cervical cancer cell lines. CaSki, C33A and HeLa cells were treated with metformin (0, 5 or 10 mM) for 48 h. Protein expression levels of PIK3CA, p-AKT, AKT, p-p70S6K, and p70S6K were (A) determined via western blotting and semi-quantified in (B) CaSki, (C) C33A and (D) HeLa cells. Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. p, phosphorylated; PIK3CA, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α; p70S6K, p70S6 kinase; CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin.

Journal: Molecular Medicine Reports

Article Title: Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells

doi: 10.3892/mmr.2020.11725

Figure Lengend Snippet: Effects of metformin on PI3K/AKT/mTOR signaling in cervical cancer cell lines. CaSki, C33A and HeLa cells were treated with metformin (0, 5 or 10 mM) for 48 h. Protein expression levels of PIK3CA, p-AKT, AKT, p-p70S6K, and p70S6K were (A) determined via western blotting and semi-quantified in (B) CaSki, (C) C33A and (D) HeLa cells. Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON. p, phosphorylated; PIK3CA, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α; p70S6K, p70S6 kinase; CON, 0 mM metformin; M5, 5 mM metformin; M10, 10 mM metformin.

Article Snippet: The CaSki, HeLa and C33A human cervical cancer cell lines were purchased from the Bioresource Collection and Research Center.

Techniques: Expressing, Western Blot

Effects of Compound C on cell viability, AMPK signaling and apoptotic signaling in cervical cancer cell lines. CaSki, C33A and HeLa cells were pre-treated with or without Compound C (1 or 5 µM; an AMPK inhibitor) for 2 h and then treated with or without 10 mM metformin for 48 h, the concentration of metformin selected for experiment was based on the cell viability assay test. (A) Cell viability was determined by performing the Cell Counting Kit-8 assay. Protein expression levels of p-AMPK, AMPK, p-p53, p53, Bcl-2 and cleaved caspase-3 were (B) determined by western blotting and semi-quantified in (C) CaSki, (D) C33A and (E) HeLa cells. Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON; † P<0.05 vs. M10. AMPK, AMP-activated protein kinase; p, phosphorylated; CON, 0 mM metformin; M10, 10 mM metformin; Com C1, 1 µM Compound C; Com C5, 5 µM Compound C; C-cas-3, cleaved caspase-3.

Journal: Molecular Medicine Reports

Article Title: Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells

doi: 10.3892/mmr.2020.11725

Figure Lengend Snippet: Effects of Compound C on cell viability, AMPK signaling and apoptotic signaling in cervical cancer cell lines. CaSki, C33A and HeLa cells were pre-treated with or without Compound C (1 or 5 µM; an AMPK inhibitor) for 2 h and then treated with or without 10 mM metformin for 48 h, the concentration of metformin selected for experiment was based on the cell viability assay test. (A) Cell viability was determined by performing the Cell Counting Kit-8 assay. Protein expression levels of p-AMPK, AMPK, p-p53, p53, Bcl-2 and cleaved caspase-3 were (B) determined by western blotting and semi-quantified in (C) CaSki, (D) C33A and (E) HeLa cells. Data are presented as the mean ± SD from three independent experiments. *P<0.05 vs. CON; † P<0.05 vs. M10. AMPK, AMP-activated protein kinase; p, phosphorylated; CON, 0 mM metformin; M10, 10 mM metformin; Com C1, 1 µM Compound C; Com C5, 5 µM Compound C; C-cas-3, cleaved caspase-3.

Article Snippet: The CaSki, HeLa and C33A human cervical cancer cell lines were purchased from the Bioresource Collection and Research Center.

Techniques: Concentration Assay, Viability Assay, Cell Counting, Expressing, Western Blot