Review



c33a  (ATCC)


Bioz Verified Symbol ATCC is a verified supplier
Bioz Manufacturer Symbol ATCC manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 96
      Buy from Supplier

    Structured Review

    ATCC c33a
    CP681301 exerted a greater inhibition on the proliferation ability of HPV-positive than HPV-negative cancer cells. (A). A schematic diagram summarises the screen process of CDK5 inhibitors against HPV-positive cancer cell lines. (B-C). CP681301 against cell proliferation of five CSEC and HNSCC, HeLa, CaSki, SCC090, <t>C33A,</t> and SAS. Representative examples of the results from 3 independent experiments. (D). The growth curve indicates the cell proliferation of HeLa cells in the presence or the absence of CP681301. This proliferation of HeLa was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (E). The growth curve indicates the cell proliferation of CaSki cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (F). The growth curve indicates the cell proliferation of C33A cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments.
    C33a, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1151 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/c33a/product/ATCC
    Average 96 stars, based on 1151 article reviews
    c33a - by Bioz Stars, 2026-03
    96/100 stars

    Images

    1) Product Images from "HPV18E6 and CDK5 virus-host interaction is a prospective therapeutic target for HPV-positive cervical cancer"

    Article Title: HPV18E6 and CDK5 virus-host interaction is a prospective therapeutic target for HPV-positive cervical cancer

    Journal: Tumour Virus Research

    doi: 10.1016/j.tvr.2026.200339

    CP681301 exerted a greater inhibition on the proliferation ability of HPV-positive than HPV-negative cancer cells. (A). A schematic diagram summarises the screen process of CDK5 inhibitors against HPV-positive cancer cell lines. (B-C). CP681301 against cell proliferation of five CSEC and HNSCC, HeLa, CaSki, SCC090, C33A, and SAS. Representative examples of the results from 3 independent experiments. (D). The growth curve indicates the cell proliferation of HeLa cells in the presence or the absence of CP681301. This proliferation of HeLa was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (E). The growth curve indicates the cell proliferation of CaSki cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (F). The growth curve indicates the cell proliferation of C33A cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments.
    Figure Legend Snippet: CP681301 exerted a greater inhibition on the proliferation ability of HPV-positive than HPV-negative cancer cells. (A). A schematic diagram summarises the screen process of CDK5 inhibitors against HPV-positive cancer cell lines. (B-C). CP681301 against cell proliferation of five CSEC and HNSCC, HeLa, CaSki, SCC090, C33A, and SAS. Representative examples of the results from 3 independent experiments. (D). The growth curve indicates the cell proliferation of HeLa cells in the presence or the absence of CP681301. This proliferation of HeLa was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (E). The growth curve indicates the cell proliferation of CaSki cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (F). The growth curve indicates the cell proliferation of C33A cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments.

    Techniques Used: Inhibition, Viability Assay

    Inhibition of CDK5 dampens cancer phenotypes of HPV-positive cervical cancer cells. (A) (i). Representative images compare the cell migration of HeLa after scratching. Cells were seeded into 6-well plates and were scratched when they reached 100% confluence, then incubated with CP681301 (0.6, 1.5 μM) or DMSO for 24 h. Cell migration was observed and recorded through time-lapse microscopy at different time points (0, 6, 12, 24 h). (ii) The bar charts compare the relative coverage of the scratched area of HeLa upon treatment with DMSO or CP681301 (n = 3). (B) (i) The representative images show the whole-well view and colony morphology of the colonies formed by HeLa cells. Cells were seeded into 0.35% agarose containing DMEM with 20% FBS and were grown for 14 days. The agarose was stained with crystal violet. The colony morphology was observed and recorded under an optical microscope at × 100 magnification. (ii) The bar charts compare the colony number of HeLa cells upon treatment with CP681301 or DMSO (n = 3). (C) (i) The representative images compare the cell invasion of HeLa cells upon treatment with CP681301 or DMSO. Cells were seeded into the invasion chamber with serum-free medium. Cell invasion was observed and recorded through an optical microscope. (ii) The bar graphs compare the relative cell invasion abilities of HeLa cells upon treatment with CP681301 and DMSO (n = 3). Error bars indicate SEM. ∗p < 0.05; ∗∗p < 0.01. ∗∗∗p < 0.001.(D) (i) The representative images compare the cell invasion of C33A cells upon treatment with CP681301 or DMSO. Cells were seeded into the invasion chamber with serum-free medium. Cell invasion was observed and recorded through an optical microscope. (ii) The bar graphs compare the relative cell invasion abilities of C33A cells upon treatment with CP681301 and DMSO (n = 3). Error bars indicate SEM. ∗p < 0.05; ∗∗p < 0.01. ∗∗∗p < 0.001.
    Figure Legend Snippet: Inhibition of CDK5 dampens cancer phenotypes of HPV-positive cervical cancer cells. (A) (i). Representative images compare the cell migration of HeLa after scratching. Cells were seeded into 6-well plates and were scratched when they reached 100% confluence, then incubated with CP681301 (0.6, 1.5 μM) or DMSO for 24 h. Cell migration was observed and recorded through time-lapse microscopy at different time points (0, 6, 12, 24 h). (ii) The bar charts compare the relative coverage of the scratched area of HeLa upon treatment with DMSO or CP681301 (n = 3). (B) (i) The representative images show the whole-well view and colony morphology of the colonies formed by HeLa cells. Cells were seeded into 0.35% agarose containing DMEM with 20% FBS and were grown for 14 days. The agarose was stained with crystal violet. The colony morphology was observed and recorded under an optical microscope at × 100 magnification. (ii) The bar charts compare the colony number of HeLa cells upon treatment with CP681301 or DMSO (n = 3). (C) (i) The representative images compare the cell invasion of HeLa cells upon treatment with CP681301 or DMSO. Cells were seeded into the invasion chamber with serum-free medium. Cell invasion was observed and recorded through an optical microscope. (ii) The bar graphs compare the relative cell invasion abilities of HeLa cells upon treatment with CP681301 and DMSO (n = 3). Error bars indicate SEM. ∗p < 0.05; ∗∗p < 0.01. ∗∗∗p < 0.001.(D) (i) The representative images compare the cell invasion of C33A cells upon treatment with CP681301 or DMSO. Cells were seeded into the invasion chamber with serum-free medium. Cell invasion was observed and recorded through an optical microscope. (ii) The bar graphs compare the relative cell invasion abilities of C33A cells upon treatment with CP681301 and DMSO (n = 3). Error bars indicate SEM. ∗p < 0.05; ∗∗p < 0.01. ∗∗∗p < 0.001.

    Techniques Used: Inhibition, Migration, Incubation, Time-lapse Microscopy, Staining, Microscopy

    CP681301 treatment destabilized E6, reduced E6AP and rescued p53. (A). HeLa and C33A cell lines were treated with CP681301 at the concentrations of 0.6 μM and 1.5 μM for 24 h. The protein extracts were subjected to Western blotting for the detection of CDK5, 18E6, E6AP, p53, and β-actin proteins. (B). CP681301 disrupted the 18E6-E6AP protein complex. The inhibition of CP681301 was detected using the GST-pull down assay, where CP681301 was incubated with the purified GST-18E6 protein and Flag-E6AP protein for 2h. After extensive washing, the bound E6AP protein was detected via Western blotting using an anti-Flag antibody. The immunoblot (IB) on the upper panel shows the interaction of E6AP with GST-18E6, while the lower panel shows the Ponceau S stained of the blot.
    Figure Legend Snippet: CP681301 treatment destabilized E6, reduced E6AP and rescued p53. (A). HeLa and C33A cell lines were treated with CP681301 at the concentrations of 0.6 μM and 1.5 μM for 24 h. The protein extracts were subjected to Western blotting for the detection of CDK5, 18E6, E6AP, p53, and β-actin proteins. (B). CP681301 disrupted the 18E6-E6AP protein complex. The inhibition of CP681301 was detected using the GST-pull down assay, where CP681301 was incubated with the purified GST-18E6 protein and Flag-E6AP protein for 2h. After extensive washing, the bound E6AP protein was detected via Western blotting using an anti-Flag antibody. The immunoblot (IB) on the upper panel shows the interaction of E6AP with GST-18E6, while the lower panel shows the Ponceau S stained of the blot.

    Techniques Used: Western Blot, Inhibition, Pull Down Assay, Incubation, Purification, Staining



    Similar Products

    c33a  (ATCC)
    96
    ATCC c33a
    CP681301 exerted a greater inhibition on the proliferation ability of HPV-positive than HPV-negative cancer cells. (A). A schematic diagram summarises the screen process of CDK5 inhibitors against HPV-positive cancer cell lines. (B-C). CP681301 against cell proliferation of five CSEC and HNSCC, HeLa, CaSki, SCC090, <t>C33A,</t> and SAS. Representative examples of the results from 3 independent experiments. (D). The growth curve indicates the cell proliferation of HeLa cells in the presence or the absence of CP681301. This proliferation of HeLa was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (E). The growth curve indicates the cell proliferation of CaSki cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (F). The growth curve indicates the cell proliferation of C33A cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments.
    C33a, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/c33a/product/ATCC
    Average 96 stars, based on 1 article reviews
    c33a - by Bioz Stars, 2026-03
    96/100 stars
    		  Buy from Supplier
    c33a cells  (ATCC)
    96
    ATCC c33a cells
    CP681301 exerted a greater inhibition on the proliferation ability of HPV-positive than HPV-negative cancer cells. (A). A schematic diagram summarises the screen process of CDK5 inhibitors against HPV-positive cancer cell lines. (B-C). CP681301 against cell proliferation of five CSEC and HNSCC, HeLa, CaSki, SCC090, <t>C33A,</t> and SAS. Representative examples of the results from 3 independent experiments. (D). The growth curve indicates the cell proliferation of HeLa cells in the presence or the absence of CP681301. This proliferation of HeLa was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (E). The growth curve indicates the cell proliferation of CaSki cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (F). The growth curve indicates the cell proliferation of C33A cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments.
    C33a Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/c33a cells/product/ATCC
    Average 96 stars, based on 1 article reviews
    c33a cells - by Bioz Stars, 2026-03
    96/100 stars
    		  Buy from Supplier

    Image Search Results


    CP681301 exerted a greater inhibition on the proliferation ability of HPV-positive than HPV-negative cancer cells. (A). A schematic diagram summarises the screen process of CDK5 inhibitors against HPV-positive cancer cell lines. (B-C). CP681301 against cell proliferation of five CSEC and HNSCC, HeLa, CaSki, SCC090, C33A, and SAS. Representative examples of the results from 3 independent experiments. (D). The growth curve indicates the cell proliferation of HeLa cells in the presence or the absence of CP681301. This proliferation of HeLa was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (E). The growth curve indicates the cell proliferation of CaSki cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (F). The growth curve indicates the cell proliferation of C33A cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments.

    Journal: Tumour Virus Research

    Article Title: HPV18E6 and CDK5 virus-host interaction is a prospective therapeutic target for HPV-positive cervical cancer

    doi: 10.1016/j.tvr.2026.200339

    Figure Lengend Snippet: CP681301 exerted a greater inhibition on the proliferation ability of HPV-positive than HPV-negative cancer cells. (A). A schematic diagram summarises the screen process of CDK5 inhibitors against HPV-positive cancer cell lines. (B-C). CP681301 against cell proliferation of five CSEC and HNSCC, HeLa, CaSki, SCC090, C33A, and SAS. Representative examples of the results from 3 independent experiments. (D). The growth curve indicates the cell proliferation of HeLa cells in the presence or the absence of CP681301. This proliferation of HeLa was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (E). The growth curve indicates the cell proliferation of CaSki cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments. (F). The growth curve indicates the cell proliferation of C33A cells in the presence or the absence of CP681301. The proliferation of CaSki was assessed using CCK8 cell viability assay. Representative examples of the results from 3 independent experiments.

    Article Snippet: HeLa (HPV18 positive cervical cancer cells), CaSki (HPV16 positive cervical cancer cells), human embryonic kidney (HEK) 293 (HPV-null epithelial cells), C33A (HPV-null cervical cancer cells), U-2 OS (HPV-null human osteosarcorma cells), SAS (HPV-null human head and neck squamous cell carcinoma cell line), and SCC090 (HPV16-positive human HNSCC cell line) were purchased from the American Type Culture Collection (ATCC) and maintained in Dulbecco's modified Eagle medium (DMEM) supplemented with 10% fetal bovine serum (FBS, GIBCO) at 37 °C in a humidified incubator with 5% CO 2 .

    Techniques: Inhibition, Viability Assay

    Inhibition of CDK5 dampens cancer phenotypes of HPV-positive cervical cancer cells. (A) (i). Representative images compare the cell migration of HeLa after scratching. Cells were seeded into 6-well plates and were scratched when they reached 100% confluence, then incubated with CP681301 (0.6, 1.5 μM) or DMSO for 24 h. Cell migration was observed and recorded through time-lapse microscopy at different time points (0, 6, 12, 24 h). (ii) The bar charts compare the relative coverage of the scratched area of HeLa upon treatment with DMSO or CP681301 (n = 3). (B) (i) The representative images show the whole-well view and colony morphology of the colonies formed by HeLa cells. Cells were seeded into 0.35% agarose containing DMEM with 20% FBS and were grown for 14 days. The agarose was stained with crystal violet. The colony morphology was observed and recorded under an optical microscope at × 100 magnification. (ii) The bar charts compare the colony number of HeLa cells upon treatment with CP681301 or DMSO (n = 3). (C) (i) The representative images compare the cell invasion of HeLa cells upon treatment with CP681301 or DMSO. Cells were seeded into the invasion chamber with serum-free medium. Cell invasion was observed and recorded through an optical microscope. (ii) The bar graphs compare the relative cell invasion abilities of HeLa cells upon treatment with CP681301 and DMSO (n = 3). Error bars indicate SEM. ∗p < 0.05; ∗∗p < 0.01. ∗∗∗p < 0.001.(D) (i) The representative images compare the cell invasion of C33A cells upon treatment with CP681301 or DMSO. Cells were seeded into the invasion chamber with serum-free medium. Cell invasion was observed and recorded through an optical microscope. (ii) The bar graphs compare the relative cell invasion abilities of C33A cells upon treatment with CP681301 and DMSO (n = 3). Error bars indicate SEM. ∗p < 0.05; ∗∗p < 0.01. ∗∗∗p < 0.001.

    Journal: Tumour Virus Research

    Article Title: HPV18E6 and CDK5 virus-host interaction is a prospective therapeutic target for HPV-positive cervical cancer

    doi: 10.1016/j.tvr.2026.200339

    Figure Lengend Snippet: Inhibition of CDK5 dampens cancer phenotypes of HPV-positive cervical cancer cells. (A) (i). Representative images compare the cell migration of HeLa after scratching. Cells were seeded into 6-well plates and were scratched when they reached 100% confluence, then incubated with CP681301 (0.6, 1.5 μM) or DMSO for 24 h. Cell migration was observed and recorded through time-lapse microscopy at different time points (0, 6, 12, 24 h). (ii) The bar charts compare the relative coverage of the scratched area of HeLa upon treatment with DMSO or CP681301 (n = 3). (B) (i) The representative images show the whole-well view and colony morphology of the colonies formed by HeLa cells. Cells were seeded into 0.35% agarose containing DMEM with 20% FBS and were grown for 14 days. The agarose was stained with crystal violet. The colony morphology was observed and recorded under an optical microscope at × 100 magnification. (ii) The bar charts compare the colony number of HeLa cells upon treatment with CP681301 or DMSO (n = 3). (C) (i) The representative images compare the cell invasion of HeLa cells upon treatment with CP681301 or DMSO. Cells were seeded into the invasion chamber with serum-free medium. Cell invasion was observed and recorded through an optical microscope. (ii) The bar graphs compare the relative cell invasion abilities of HeLa cells upon treatment with CP681301 and DMSO (n = 3). Error bars indicate SEM. ∗p < 0.05; ∗∗p < 0.01. ∗∗∗p < 0.001.(D) (i) The representative images compare the cell invasion of C33A cells upon treatment with CP681301 or DMSO. Cells were seeded into the invasion chamber with serum-free medium. Cell invasion was observed and recorded through an optical microscope. (ii) The bar graphs compare the relative cell invasion abilities of C33A cells upon treatment with CP681301 and DMSO (n = 3). Error bars indicate SEM. ∗p < 0.05; ∗∗p < 0.01. ∗∗∗p < 0.001.

    Article Snippet: HeLa (HPV18 positive cervical cancer cells), CaSki (HPV16 positive cervical cancer cells), human embryonic kidney (HEK) 293 (HPV-null epithelial cells), C33A (HPV-null cervical cancer cells), U-2 OS (HPV-null human osteosarcorma cells), SAS (HPV-null human head and neck squamous cell carcinoma cell line), and SCC090 (HPV16-positive human HNSCC cell line) were purchased from the American Type Culture Collection (ATCC) and maintained in Dulbecco's modified Eagle medium (DMEM) supplemented with 10% fetal bovine serum (FBS, GIBCO) at 37 °C in a humidified incubator with 5% CO 2 .

    Techniques: Inhibition, Migration, Incubation, Time-lapse Microscopy, Staining, Microscopy

    CP681301 treatment destabilized E6, reduced E6AP and rescued p53. (A). HeLa and C33A cell lines were treated with CP681301 at the concentrations of 0.6 μM and 1.5 μM for 24 h. The protein extracts were subjected to Western blotting for the detection of CDK5, 18E6, E6AP, p53, and β-actin proteins. (B). CP681301 disrupted the 18E6-E6AP protein complex. The inhibition of CP681301 was detected using the GST-pull down assay, where CP681301 was incubated with the purified GST-18E6 protein and Flag-E6AP protein for 2h. After extensive washing, the bound E6AP protein was detected via Western blotting using an anti-Flag antibody. The immunoblot (IB) on the upper panel shows the interaction of E6AP with GST-18E6, while the lower panel shows the Ponceau S stained of the blot.

    Journal: Tumour Virus Research

    Article Title: HPV18E6 and CDK5 virus-host interaction is a prospective therapeutic target for HPV-positive cervical cancer

    doi: 10.1016/j.tvr.2026.200339

    Figure Lengend Snippet: CP681301 treatment destabilized E6, reduced E6AP and rescued p53. (A). HeLa and C33A cell lines were treated with CP681301 at the concentrations of 0.6 μM and 1.5 μM for 24 h. The protein extracts were subjected to Western blotting for the detection of CDK5, 18E6, E6AP, p53, and β-actin proteins. (B). CP681301 disrupted the 18E6-E6AP protein complex. The inhibition of CP681301 was detected using the GST-pull down assay, where CP681301 was incubated with the purified GST-18E6 protein and Flag-E6AP protein for 2h. After extensive washing, the bound E6AP protein was detected via Western blotting using an anti-Flag antibody. The immunoblot (IB) on the upper panel shows the interaction of E6AP with GST-18E6, while the lower panel shows the Ponceau S stained of the blot.

    Article Snippet: HeLa (HPV18 positive cervical cancer cells), CaSki (HPV16 positive cervical cancer cells), human embryonic kidney (HEK) 293 (HPV-null epithelial cells), C33A (HPV-null cervical cancer cells), U-2 OS (HPV-null human osteosarcorma cells), SAS (HPV-null human head and neck squamous cell carcinoma cell line), and SCC090 (HPV16-positive human HNSCC cell line) were purchased from the American Type Culture Collection (ATCC) and maintained in Dulbecco's modified Eagle medium (DMEM) supplemented with 10% fetal bovine serum (FBS, GIBCO) at 37 °C in a humidified incubator with 5% CO 2 .

    Techniques: Western Blot, Inhibition, Pull Down Assay, Incubation, Purification, Staining