Review

cervical cancer derived cell line siha (ATCC)

Name: cervical cancer derived cell line siha
Brand: ATCC
Rating: 99 (2610 reviews)

ATCC is a verified supplier

ATCC manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

ATCC cervical cancer derived cell line siha

A stable clone of HPV-16 E6/ E7 expressing <t>human</t> <t>cervical</t> cancer <t>SiHa</t> cells with a p53-Luciferase (p53-Luc) reporter and a clone of HPV-negative RPE-1 cells expressing the same p53-Luc reporter were incubated with DMSO (0.02% (v/v)) or increasing concentrations of compounds added to the media. SiHa-P53-Luc cells (red) and RPE-luc cells (blue) were treated with increasing concentrations of (A) KTI-218 or (B) KT-240 for 24 hrs. To study the contribution of the covalent warhead, we prepared, KTI-239, an analog of KTI-218 that lacks the acrylamide warhead and tested in SiHa-P53-Luc (C) and RPE-luc cells (D ), respectively. Structures of each compound is shown in the insets. Luciferase and cell viability were measured after 24 hours. Luc signal was normalized to cell viability and p53-Luc induction is expressed as fold-change over DMSO control. Data is expressed as S.E.M and each experiment was completed at least three independent times (n ≥ 3).

Cervical Cancer Derived Cell Line Siha, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 2610 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/cervical cancer derived cell line siha/product/ATCC
Average 99 stars, based on 2610 article reviews

cervical cancer derived cell line siha - by Bioz Stars, 2026-02

99/100 stars

Images

1) Product Images from "Covalent Inhibition of the Human Papillomavirus Type 16 E6 Protein Restores p53 and Suppresses HPV-Driven Tumorigenesis"

Article Title: Covalent Inhibition of the Human Papillomavirus Type 16 E6 Protein Restores p53 and Suppresses HPV-Driven Tumorigenesis

Journal: bioRxiv

doi: 10.1101/2025.08.24.671874

A stable clone of HPV-16 E6/ E7 expressing human cervical cancer SiHa cells with a p53-Luciferase (p53-Luc) reporter and a clone of HPV-negative RPE-1 cells expressing the same p53-Luc reporter were incubated with DMSO (0.02% (v/v)) or increasing concentrations of compounds added to the media. SiHa-P53-Luc cells (red) and RPE-luc cells (blue) were treated with increasing concentrations of (A) KTI-218 or (B) KT-240 for 24 hrs. To study the contribution of the covalent warhead, we prepared, KTI-239, an analog of KTI-218 that lacks the acrylamide warhead and tested in SiHa-P53-Luc (C) and RPE-luc cells (D ), respectively. Structures of each compound is shown in the insets. Luciferase and cell viability were measured after 24 hours. Luc signal was normalized to cell viability and p53-Luc induction is expressed as fold-change over DMSO control. Data is expressed as S.E.M and each experiment was completed at least three independent times (n ≥ 3).

Figure Legend Snippet: A stable clone of HPV-16 E6/ E7 expressing human cervical cancer SiHa cells with a p53-Luciferase (p53-Luc) reporter and a clone of HPV-negative RPE-1 cells expressing the same p53-Luc reporter were incubated with DMSO (0.02% (v/v)) or increasing concentrations of compounds added to the media. SiHa-P53-Luc cells (red) and RPE-luc cells (blue) were treated with increasing concentrations of (A) KTI-218 or (B) KT-240 for 24 hrs. To study the contribution of the covalent warhead, we prepared, KTI-239, an analog of KTI-218 that lacks the acrylamide warhead and tested in SiHa-P53-Luc (C) and RPE-luc cells (D ), respectively. Structures of each compound is shown in the insets. Luciferase and cell viability were measured after 24 hours. Luc signal was normalized to cell viability and p53-Luc induction is expressed as fold-change over DMSO control. Data is expressed as S.E.M and each experiment was completed at least three independent times (n ≥ 3).

Techniques Used: Stable Transfection, Expressing, Luciferase, Incubation, Control

SiHa, SiHa C51S, and RPE-1 cells were cultured in KTI-240 (5 µM), DMSO or etoposide (ETO, 25 µM) for 16 hours, cells were lysed, proteins extracted and subjected to Western blot analysis. A) KTI-240 increased p21 levels without affecting p16 protein. (B) E6AP and MDM2 protein levels were not changed after KTI-240 treatment. p53 protein was included as a positive control. KTI-240 decreased Foxm1 and Rb protein expression in SiHa and C51S cells but not RPE-1, while Puma increased only in SiHa cells. The heatmaps in (E) and (F) summarize the detected changes at the mRNA and protein level. (G, H) E6 protein levels were significantly decreased in SiHa cells, while E7 was unchanged in both HPV+ cell lines. Protein expression was normalized to GAPDH and expressed as fold-change. Data was expressed as S.E.M and analyzed using one-way ANOVA with Dunnett’s or Bonferroni post hoc analysis were applicable. Experiments were repeated at least three independent times (n ≥ 3; * p < 0.05).

Figure Legend Snippet: SiHa, SiHa C51S, and RPE-1 cells were cultured in KTI-240 (5 µM), DMSO or etoposide (ETO, 25 µM) for 16 hours, cells were lysed, proteins extracted and subjected to Western blot analysis. A) KTI-240 increased p21 levels without affecting p16 protein. (B) E6AP and MDM2 protein levels were not changed after KTI-240 treatment. p53 protein was included as a positive control. KTI-240 decreased Foxm1 and Rb protein expression in SiHa and C51S cells but not RPE-1, while Puma increased only in SiHa cells. The heatmaps in (E) and (F) summarize the detected changes at the mRNA and protein level. (G, H) E6 protein levels were significantly decreased in SiHa cells, while E7 was unchanged in both HPV+ cell lines. Protein expression was normalized to GAPDH and expressed as fold-change. Data was expressed as S.E.M and analyzed using one-way ANOVA with Dunnett’s or Bonferroni post hoc analysis were applicable. Experiments were repeated at least three independent times (n ≥ 3; * p < 0.05).

Techniques Used: Cell Culture, Western Blot, Positive Control, Expressing

SiHa, SiHa C51S, and RPE-1 cells were cultured in KTI-240 for 16 hours and RNA was extracted and sequenced from three independent experiments. (A, B) . Parallel cell cultures were analyzed for p53 protein levels by western blots showing a robust induction of p53. Data presented as S.E.M (n=3; * p<0.05). (C-H) . Differentially expressed genes were identified using DESeq2 analysis with a false discovery rate of <0.01 and a fold change of >2. Volcano plots showing significant transcriptional increases (right, red) and decreases (left, blue) comparing vehicle vs. KTI-240 treated cells. HPV-16 E6 and E7 mRNAs were detected and did not differ between WT and C51S SiHa cells lines. ( F, H ). TP53 mRNA was unchanged in all three cell lines upon KTI-240 treatment. Increased expression of p53 regulated genes occurred only in wild-type SiHa but not C51S or RPE-1 cells ( F, G, H ). p53 protein expression was normalized to GAPDH and expressed as fold-change. Data is expressed as S.E.M and was analyzed with one-way ANOVA with Dunnett’s or Bonferroni post hoc analysis. Each experiment was completed three independent times (n = 3; * p < 0.05).

Figure Legend Snippet: SiHa, SiHa C51S, and RPE-1 cells were cultured in KTI-240 for 16 hours and RNA was extracted and sequenced from three independent experiments. (A, B) . Parallel cell cultures were analyzed for p53 protein levels by western blots showing a robust induction of p53. Data presented as S.E.M (n=3; * p<0.05). (C-H) . Differentially expressed genes were identified using DESeq2 analysis with a false discovery rate of <0.01 and a fold change of >2. Volcano plots showing significant transcriptional increases (right, red) and decreases (left, blue) comparing vehicle vs. KTI-240 treated cells. HPV-16 E6 and E7 mRNAs were detected and did not differ between WT and C51S SiHa cells lines. ( F, H ). TP53 mRNA was unchanged in all three cell lines upon KTI-240 treatment. Increased expression of p53 regulated genes occurred only in wild-type SiHa but not C51S or RPE-1 cells ( F, G, H ). p53 protein expression was normalized to GAPDH and expressed as fold-change. Data is expressed as S.E.M and was analyzed with one-way ANOVA with Dunnett’s or Bonferroni post hoc analysis. Each experiment was completed three independent times (n = 3; * p < 0.05).

Techniques Used: Cell Culture, Western Blot, Expressing

(A) HPV+ cervical cancer cell lines, SiHa and CaSki, the oral cancer derived lines UM-SCC-47 and UM-SCC-104, and RPE-1 were incubated with increasing concentrations of KTI-218 or DMSO for 24 hours and cell viability was analyzed by Calcein-AM assay. (B) HPV negative RPE-1, human foreskin keratinocytes (HFK) and C51S mutant cells were analyzed for their cell viability after KTI-218 treatment. (C, D) cell viability of SiHa, CaSki, SCC-47, SCC-104, SiHa C51S, and RPE-1, HFK and normal oral keratinocytes was assessed after KTI-240 or DMSO treatment with for 48 hours. Cell viability is expressed as a percent change over DMSO control-treated cells. Data expressed as S.E.M and each experiment was completed at least three independent times (n ≥ 3).

Figure Legend Snippet: (A) HPV+ cervical cancer cell lines, SiHa and CaSki, the oral cancer derived lines UM-SCC-47 and UM-SCC-104, and RPE-1 were incubated with increasing concentrations of KTI-218 or DMSO for 24 hours and cell viability was analyzed by Calcein-AM assay. (B) HPV negative RPE-1, human foreskin keratinocytes (HFK) and C51S mutant cells were analyzed for their cell viability after KTI-218 treatment. (C, D) cell viability of SiHa, CaSki, SCC-47, SCC-104, SiHa C51S, and RPE-1, HFK and normal oral keratinocytes was assessed after KTI-240 or DMSO treatment with for 48 hours. Cell viability is expressed as a percent change over DMSO control-treated cells. Data expressed as S.E.M and each experiment was completed at least three independent times (n ≥ 3).

Techniques Used: Derivative Assay, Incubation, Calcein AM Assay, Mutagenesis, Control

( A, B ) Nu/Nu mice were injected subcutaneously with HPV-16+ SCC-UM-47 cancer cells. Intraperitoneal injections of 50 mg/kg KTI-218 (n=8, green) or vehicle (VH, n=7 black) began when tumors were ∼50-100 mm 3 . Tumor size was measured by calipers and expressed as S.E.M. and analyzed using two-way ANOVA (p<0.01). Representative mice and extracted tumors are shown in ( B ). Nu/Nu mice were injected subcutaneously with HPV-16+ SiHa cancer cells stably expressing a Luciferase construct ( C ). Intraperitoneal (IP) injections of 50 mg/kg KTI-218 (n=5, green) or vehicle (VH, n=4 black) began when all tumors had a bioluminescent signal. Bioluminescence was measured using a IVIS SpectrumCT optical imaging system ( D ). Representative tumors and tumor weights are shown in ( E ). Nu/Nu mice were injected subcutaneously (SC) with ( F ) HPV-negative cervical cancer cell line C33a or ( G ) HPV + SiHa C51S cells. Intraperitoneal injections of 50 mg/kg KTI-218 began when tumors were ∼50-100 mm 3 . ( H ) Nu/Nu mice were injected SC with HPV-16+ SCC-UM-47 cancer cells. IP injections of 50 mg/kg KTI-240 (n=10, green) or vehicle (VH, n=9 black) began when tumors were ∼50-100 mm 3 . Data expressed as S.E.M and analyzed using two-way ANOVA; * p <0.05.

Figure Legend Snippet: ( A, B ) Nu/Nu mice were injected subcutaneously with HPV-16+ SCC-UM-47 cancer cells. Intraperitoneal injections of 50 mg/kg KTI-218 (n=8, green) or vehicle (VH, n=7 black) began when tumors were ∼50-100 mm 3 . Tumor size was measured by calipers and expressed as S.E.M. and analyzed using two-way ANOVA (p<0.01). Representative mice and extracted tumors are shown in ( B ). Nu/Nu mice were injected subcutaneously with HPV-16+ SiHa cancer cells stably expressing a Luciferase construct ( C ). Intraperitoneal (IP) injections of 50 mg/kg KTI-218 (n=5, green) or vehicle (VH, n=4 black) began when all tumors had a bioluminescent signal. Bioluminescence was measured using a IVIS SpectrumCT optical imaging system ( D ). Representative tumors and tumor weights are shown in ( E ). Nu/Nu mice were injected subcutaneously (SC) with ( F ) HPV-negative cervical cancer cell line C33a or ( G ) HPV + SiHa C51S cells. Intraperitoneal injections of 50 mg/kg KTI-218 began when tumors were ∼50-100 mm 3 . ( H ) Nu/Nu mice were injected SC with HPV-16+ SCC-UM-47 cancer cells. IP injections of 50 mg/kg KTI-240 (n=10, green) or vehicle (VH, n=9 black) began when tumors were ∼50-100 mm 3 . Data expressed as S.E.M and analyzed using two-way ANOVA; * p <0.05.

Techniques Used: Injection, Stable Transfection, Expressing, Luciferase, Construct, Optical Imaging

Image Search Results

Journal: bioRxiv

Article Title: Covalent Inhibition of the Human Papillomavirus Type 16 E6 Protein Restores p53 and Suppresses HPV-Driven Tumorigenesis

doi: 10.1101/2025.08.24.671874

Figure Lengend Snippet: A stable clone of HPV-16 E6/ E7 expressing human cervical cancer SiHa cells with a p53-Luciferase (p53-Luc) reporter and a clone of HPV-negative RPE-1 cells expressing the same p53-Luc reporter were incubated with DMSO (0.02% (v/v)) or increasing concentrations of compounds added to the media. SiHa-P53-Luc cells (red) and RPE-luc cells (blue) were treated with increasing concentrations of (A) KTI-218 or (B) KT-240 for 24 hrs. To study the contribution of the covalent warhead, we prepared, KTI-239, an analog of KTI-218 that lacks the acrylamide warhead and tested in SiHa-P53-Luc (C) and RPE-luc cells (D ), respectively. Structures of each compound is shown in the insets. Luciferase and cell viability were measured after 24 hours. Luc signal was normalized to cell viability and p53-Luc induction is expressed as fold-change over DMSO control. Data is expressed as S.E.M and each experiment was completed at least three independent times (n ≥ 3).

Article Snippet: These DNA constructs were transfected into HPV16 expressing human cervical cancer derived cell line SiHa (ATCC-HTB35TM), which was selected because levels of E6 and E7 are directed by the native HPV16 promoter.

Techniques: Stable Transfection, Expressing, Luciferase, Incubation, Control

Journal: bioRxiv

Article Title: Covalent Inhibition of the Human Papillomavirus Type 16 E6 Protein Restores p53 and Suppresses HPV-Driven Tumorigenesis

doi: 10.1101/2025.08.24.671874

Figure Lengend Snippet: SiHa, SiHa C51S, and RPE-1 cells were cultured in KTI-240 (5 µM), DMSO or etoposide (ETO, 25 µM) for 16 hours, cells were lysed, proteins extracted and subjected to Western blot analysis. A) KTI-240 increased p21 levels without affecting p16 protein. (B) E6AP and MDM2 protein levels were not changed after KTI-240 treatment. p53 protein was included as a positive control. KTI-240 decreased Foxm1 and Rb protein expression in SiHa and C51S cells but not RPE-1, while Puma increased only in SiHa cells. The heatmaps in (E) and (F) summarize the detected changes at the mRNA and protein level. (G, H) E6 protein levels were significantly decreased in SiHa cells, while E7 was unchanged in both HPV+ cell lines. Protein expression was normalized to GAPDH and expressed as fold-change. Data was expressed as S.E.M and analyzed using one-way ANOVA with Dunnett’s or Bonferroni post hoc analysis were applicable. Experiments were repeated at least three independent times (n ≥ 3; * p < 0.05).

Techniques: Cell Culture, Western Blot, Positive Control, Expressing

Journal: bioRxiv

Article Title: Covalent Inhibition of the Human Papillomavirus Type 16 E6 Protein Restores p53 and Suppresses HPV-Driven Tumorigenesis

doi: 10.1101/2025.08.24.671874

Figure Lengend Snippet: SiHa, SiHa C51S, and RPE-1 cells were cultured in KTI-240 for 16 hours and RNA was extracted and sequenced from three independent experiments. (A, B) . Parallel cell cultures were analyzed for p53 protein levels by western blots showing a robust induction of p53. Data presented as S.E.M (n=3; * p<0.05). (C-H) . Differentially expressed genes were identified using DESeq2 analysis with a false discovery rate of <0.01 and a fold change of >2. Volcano plots showing significant transcriptional increases (right, red) and decreases (left, blue) comparing vehicle vs. KTI-240 treated cells. HPV-16 E6 and E7 mRNAs were detected and did not differ between WT and C51S SiHa cells lines. ( F, H ). TP53 mRNA was unchanged in all three cell lines upon KTI-240 treatment. Increased expression of p53 regulated genes occurred only in wild-type SiHa but not C51S or RPE-1 cells ( F, G, H ). p53 protein expression was normalized to GAPDH and expressed as fold-change. Data is expressed as S.E.M and was analyzed with one-way ANOVA with Dunnett’s or Bonferroni post hoc analysis. Each experiment was completed three independent times (n = 3; * p < 0.05).

Techniques: Cell Culture, Western Blot, Expressing

Journal: bioRxiv

Article Title: Covalent Inhibition of the Human Papillomavirus Type 16 E6 Protein Restores p53 and Suppresses HPV-Driven Tumorigenesis

doi: 10.1101/2025.08.24.671874

Figure Lengend Snippet: (A) HPV+ cervical cancer cell lines, SiHa and CaSki, the oral cancer derived lines UM-SCC-47 and UM-SCC-104, and RPE-1 were incubated with increasing concentrations of KTI-218 or DMSO for 24 hours and cell viability was analyzed by Calcein-AM assay. (B) HPV negative RPE-1, human foreskin keratinocytes (HFK) and C51S mutant cells were analyzed for their cell viability after KTI-218 treatment. (C, D) cell viability of SiHa, CaSki, SCC-47, SCC-104, SiHa C51S, and RPE-1, HFK and normal oral keratinocytes was assessed after KTI-240 or DMSO treatment with for 48 hours. Cell viability is expressed as a percent change over DMSO control-treated cells. Data expressed as S.E.M and each experiment was completed at least three independent times (n ≥ 3).

Techniques: Derivative Assay, Incubation, Calcein AM Assay, Mutagenesis, Control

Journal: bioRxiv

Article Title: Covalent Inhibition of the Human Papillomavirus Type 16 E6 Protein Restores p53 and Suppresses HPV-Driven Tumorigenesis

doi: 10.1101/2025.08.24.671874

Figure Lengend Snippet: ( A, B ) Nu/Nu mice were injected subcutaneously with HPV-16+ SCC-UM-47 cancer cells. Intraperitoneal injections of 50 mg/kg KTI-218 (n=8, green) or vehicle (VH, n=7 black) began when tumors were ∼50-100 mm 3 . Tumor size was measured by calipers and expressed as S.E.M. and analyzed using two-way ANOVA (p<0.01). Representative mice and extracted tumors are shown in ( B ). Nu/Nu mice were injected subcutaneously with HPV-16+ SiHa cancer cells stably expressing a Luciferase construct ( C ). Intraperitoneal (IP) injections of 50 mg/kg KTI-218 (n=5, green) or vehicle (VH, n=4 black) began when all tumors had a bioluminescent signal. Bioluminescence was measured using a IVIS SpectrumCT optical imaging system ( D ). Representative tumors and tumor weights are shown in ( E ). Nu/Nu mice were injected subcutaneously (SC) with ( F ) HPV-negative cervical cancer cell line C33a or ( G ) HPV + SiHa C51S cells. Intraperitoneal injections of 50 mg/kg KTI-218 began when tumors were ∼50-100 mm 3 . ( H ) Nu/Nu mice were injected SC with HPV-16+ SCC-UM-47 cancer cells. IP injections of 50 mg/kg KTI-240 (n=10, green) or vehicle (VH, n=9 black) began when tumors were ∼50-100 mm 3 . Data expressed as S.E.M and analyzed using two-way ANOVA; * p <0.05.

Techniques: Injection, Stable Transfection, Expressing, Luciferase, Construct, Optical Imaging

Relative expression of GRPR mRNA by real time PCR: Relative expression of GRPR mRNA in (A) normal keratinocytes (PHK) and cervical cancer-derived cell lines (C33, SiHa and HeLa) and (B) keratinocytes transduced with the empty vector (pLXSN Ø) or with the vector containing HPV16 oncogenes E6 and/or E7

Journal: Revista Brasileira de Ginecologia e Obstetrícia

Article Title: Gastrin-releasing peptide receptor: a promising new biomarker to identify cervical precursor lesions and cancer

doi: 10.61622/rbgo/2025rbgo4

Figure Lengend Snippet: Relative expression of GRPR mRNA by real time PCR: Relative expression of GRPR mRNA in (A) normal keratinocytes (PHK) and cervical cancer-derived cell lines (C33, SiHa and HeLa) and (B) keratinocytes transduced with the empty vector (pLXSN Ø) or with the vector containing HPV16 oncogenes E6 and/or E7

Article Snippet: Cervical cancer-derived cell lines SiHa (HPV16, ATCC #HTB-35), HeLa (HPV18, ATCC #CCL-2) and C33 (HPV negative, ATCC #HTB-31) were cultured in Eagle's minimal essential medium (MEM) (Invitrogen, Carlsbad, CA, USA) supplemented with 10% bovine fetal serum (BFS) (Cultilab, Campinas, SP, Brazil) and maintained at 37°C and 5% CO 2 .

Techniques: Expressing, Real-time Polymerase Chain Reaction, Derivative Assay, Transduction, Plasmid Preparation

Review

Structured Review

Images

1) Product Images from "Covalent Inhibition of the Human Papillomavirus Type 16 E6 Protein Restores p53 and Suppresses HPV-Driven Tumorigenesis"

Similar Products

Image Search Results