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siha human cervix cancer cells (ATCC)

Name: siha human cervix cancer cells
Brand: ATCC
Rating: 99 (2611 reviews)

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ATCC siha human cervix cancer cells

a – c Cancer cells were treated with increasing doses of MitoQ for 24 h, and the oxygen consumption rate (OCR) of 10 000 cells/well was measured using Seahorse oximetry. Left graphs represent total OCR measurements over time. From Seahorse traces, basal, maximal and ATP-linked mitochondrial OCRs (mtOCRs) were calculated and are displayed on the right. a <t>SiHa</t> human cervix cancer cells were tested ( n = 4). <t>b</t> <t>PC3</t> human prostate cancer cells were tested ( n = 4). Full mtOCR inhibition was reached at 250 nM MitoQ (arrow). c HCT116 human prostate cancer cells were tested ( n = 4). Full mtOCR inhibition was reached at 250 nM MitoQ (arrow). All data are shown as means ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.005 by one-way ANOVA with Dunnett’s multiple comparisons test.

Siha Human Cervix Cancer Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 2611 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 99 stars, based on 2611 article reviews

siha human cervix cancer cells - by Bioz Stars, 2026-03

99/100 stars

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Article Title: Mitochondria-targeted antioxidant MitoQ radiosensitizes tumors by decreasing mitochondrial oxygen consumption

Journal: Cell Death Discovery

doi: 10.1038/s41420-024-02277-9

Figure Legend Snippet: a – c Cancer cells were treated with increasing doses of MitoQ for 24 h, and the oxygen consumption rate (OCR) of 10 000 cells/well was measured using Seahorse oximetry. Left graphs represent total OCR measurements over time. From Seahorse traces, basal, maximal and ATP-linked mitochondrial OCRs (mtOCRs) were calculated and are displayed on the right. a SiHa human cervix cancer cells were tested ( n = 4). b PC3 human prostate cancer cells were tested ( n = 4). Full mtOCR inhibition was reached at 250 nM MitoQ (arrow). c HCT116 human prostate cancer cells were tested ( n = 4). Full mtOCR inhibition was reached at 250 nM MitoQ (arrow). All data are shown as means ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.005 by one-way ANOVA with Dunnett’s multiple comparisons test.

Techniques Used: Inhibition

$a MCF7 breast cancer cells were treated ± 500 nM MitoQ for 24 h and subjected to subcellular fractionation. Mitochondrial and cytosolic ATP were measured using a fluorescence assay and are reported in the left and right graphs, respectively ( n = 3). b MCF7 cells were treated with increasing doses of MitoQ for 24 h, and ΔΨ was measured via JC-10 fluorescence ( n = 6). c Glucose consumption and lactate production rates were measured in MCF7 cells pretreated for 24 h ± 500 nM MitoQ ( n = 6). d As in (a) but using MDA-MB-231 cancer cells treated ± 250 nM MitoQ ( n = 3). e As in (b) but using MDA-MB-231 cells ( n = 6). f As in c but using MDA-MB-231 cancer cells treated ± 250 nM MitoQ ( n = 6). g Seahorse XF cell energy map of cancer cells plotted by their basal OCR and basal extracellular acidification rate (ECAR) before and 24 h after treatment with MitoQ at the concentrations identified to bring ATP production linked to mtOCR to 0 (SiHa, 1 µM; MCF7, 500 nM; MDA-MB-231, 250 nM; PC3, 250 nM; HCT116, 250 nM) ( n = 4–6). All data are shown as means ± SEM. ns P > 0.05, ** P < 0.01, *** P < 0.005 compared to untreated controls; by one-way ANOVA with Tukey’s multiple comparisons test ( a, b, d, e ) or Student’s t test ( c, f ).$
Figure Legend Snippet: a MCF7 breast cancer cells were treated ± 500 nM MitoQ for 24 h and subjected to subcellular fractionation. Mitochondrial and cytosolic ATP were measured using a fluorescence assay and are reported in the left and right graphs, respectively ( n = 3). b MCF7 cells were treated with increasing doses of MitoQ for 24 h, and ΔΨ was measured via JC-10 fluorescence ( n = 6). c Glucose consumption and lactate production rates were measured in MCF7 cells pretreated for 24 h ± 500 nM MitoQ ( n = 6). d As in (a) but using MDA-MB-231 cancer cells treated ± 250 nM MitoQ ( n = 3). e As in (b) but using MDA-MB-231 cells ( n = 6). f As in c but using MDA-MB-231 cancer cells treated ± 250 nM MitoQ ( n = 6). g Seahorse XF cell energy map of cancer cells plotted by their basal OCR and basal extracellular acidification rate (ECAR) before and 24 h after treatment with MitoQ at the concentrations identified to bring ATP production linked to mtOCR to 0 (SiHa, 1 µM; MCF7, 500 nM; MDA-MB-231, 250 nM; PC3, 250 nM; HCT116, 250 nM) ( n = 4–6). All data are shown as means ± SEM. ns P > 0.05, ** P < 0.01, *** P < 0.005 compared to untreated controls; by one-way ANOVA with Tukey’s multiple comparisons test ( a, b, d, e ) or Student’s t test ( c, f ).

Techniques Used: Fractionation, Fluorescence

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Journal: Cell Death Discovery

Article Title: Mitochondria-targeted antioxidant MitoQ radiosensitizes tumors by decreasing mitochondrial oxygen consumption

doi: 10.1038/s41420-024-02277-9

Figure Lengend Snippet: a – c Cancer cells were treated with increasing doses of MitoQ for 24 h, and the oxygen consumption rate (OCR) of 10 000 cells/well was measured using Seahorse oximetry. Left graphs represent total OCR measurements over time. From Seahorse traces, basal, maximal and ATP-linked mitochondrial OCRs (mtOCRs) were calculated and are displayed on the right. a SiHa human cervix cancer cells were tested ( n = 4). b PC3 human prostate cancer cells were tested ( n = 4). Full mtOCR inhibition was reached at 250 nM MitoQ (arrow). c HCT116 human prostate cancer cells were tested ( n = 4). Full mtOCR inhibition was reached at 250 nM MitoQ (arrow). All data are shown as means ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.005 by one-way ANOVA with Dunnett’s multiple comparisons test.

Article Snippet: MCF7 (American Type Culture Collection [ATCC], Manassas, VA, USA; catalog #HTB-22) and MDA-MB-231 (ATCC, catalogue #HTB-26) human breast adenocarcinoma cancer cells, SiHa human cervix cancer cells (ATCC, catalog #HTB-35), PC3 human prostate cancer cells (ATCC, catalog #CRL-1435) and HCT116 human colon cancer cells (ATCC, catalog #CCL-247) were cultured at 37 °C in a 5% CO 2 humidity-controled incubator in DMEM containing GlutaMAX, 4.5 g/L D -glucose without pyruvate (ThermoFisher Scientific, Dilbeek, Belgium; catalogue #10566016), supplemented with 10% FBS (Sigma-Aldrich, Overijse, Belgium).

Techniques: Inhibition

Journal: Cell Death Discovery

Article Title: Mitochondria-targeted antioxidant MitoQ radiosensitizes tumors by decreasing mitochondrial oxygen consumption

doi: 10.1038/s41420-024-02277-9

Figure Lengend Snippet: a MCF7 breast cancer cells were treated ± 500 nM MitoQ for 24 h and subjected to subcellular fractionation. Mitochondrial and cytosolic ATP were measured using a fluorescence assay and are reported in the left and right graphs, respectively ( n = 3). b MCF7 cells were treated with increasing doses of MitoQ for 24 h, and ΔΨ was measured via JC-10 fluorescence ( n = 6). c Glucose consumption and lactate production rates were measured in MCF7 cells pretreated for 24 h ± 500 nM MitoQ ( n = 6). d As in (a) but using MDA-MB-231 cancer cells treated ± 250 nM MitoQ ( n = 3). e As in (b) but using MDA-MB-231 cells ( n = 6). f As in c but using MDA-MB-231 cancer cells treated ± 250 nM MitoQ ( n = 6). g Seahorse XF cell energy map of cancer cells plotted by their basal OCR and basal extracellular acidification rate (ECAR) before and 24 h after treatment with MitoQ at the concentrations identified to bring ATP production linked to mtOCR to 0 (SiHa, 1 µM; MCF7, 500 nM; MDA-MB-231, 250 nM; PC3, 250 nM; HCT116, 250 nM) ( n = 4–6). All data are shown as means ± SEM. ns P > 0.05, ** P < 0.01, *** P < 0.005 compared to untreated controls; by one-way ANOVA with Tukey’s multiple comparisons test ( a, b, d, e ) or Student’s t test ( c, f ).

Techniques: Fractionation, Fluorescence

Effect of CXB and DMC combinations on HeLa (A), SiHa (B) and T3T (C) cell growth. The indicated drugs were added at the following concentrations: CXB (5 μM); CXB (5 μM)/CP (2 μM); CXB (5 μM)/PA (15 μM); DMC (15 μM), DMC (15 μM)/CP (5 μM) or DMC (15 μM)/PA (20 μM). Cells were exposed to the drugs for 24 h. Data shown represent the mean ± S.D. of at least three different preparations. *p < 0.05 vs . control (non-treated cells); **p < 0.05 vs . CXB or DMC.

Journal: PLOS ONE

Article Title: Synergistic celecoxib and dimethyl-celecoxib combinations block cervix cancer growth through multiple mechanisms

doi: 10.1371/journal.pone.0308233

Figure Lengend Snippet: Effect of CXB and DMC combinations on HeLa (A), SiHa (B) and T3T (C) cell growth. The indicated drugs were added at the following concentrations: CXB (5 μM); CXB (5 μM)/CP (2 μM); CXB (5 μM)/PA (15 μM); DMC (15 μM), DMC (15 μM)/CP (5 μM) or DMC (15 μM)/PA (20 μM). Cells were exposed to the drugs for 24 h. Data shown represent the mean ± S.D. of at least three different preparations. *p < 0.05 vs . control (non-treated cells); **p < 0.05 vs . CXB or DMC.

Article Snippet: Human HeLa and SiHa cervix cancer cells were obtained from the ATCC (American Type Culture Collection).

Techniques: Control

Effect of CXB and DMC combinations on HeLa (A) and SiHa (B) energy metabolism fluxes. For A, data shown represent the mean ± S.D. of 7 different preparations. For B, data shown represent the mean ± S.D. of at least three different preparations. *p < 0.05 vs. control (non-treated cells);**p < 0.05 vs . CXB or DMC.

Journal: PLOS ONE

Article Title: Synergistic celecoxib and dimethyl-celecoxib combinations block cervix cancer growth through multiple mechanisms

doi: 10.1371/journal.pone.0308233

Figure Lengend Snippet: Effect of CXB and DMC combinations on HeLa (A) and SiHa (B) energy metabolism fluxes. For A, data shown represent the mean ± S.D. of 7 different preparations. For B, data shown represent the mean ± S.D. of at least three different preparations. *p < 0.05 vs. control (non-treated cells);**p < 0.05 vs . CXB or DMC.

Article Snippet: Human HeLa and SiHa cervix cancer cells were obtained from the ATCC (American Type Culture Collection).

Techniques: Control

Effect of CXB and DMC combinations on ROS production (A) in HeLa and ROS content (B) in SiHa cells. Data shown represent the mean ± S.D. of at least three different preparations. *p < 0.05 vs . control (non-treated cells); **p < 0.05 vs . CXB or DMC.

Journal: PLOS ONE

Article Title: Synergistic celecoxib and dimethyl-celecoxib combinations block cervix cancer growth through multiple mechanisms

doi: 10.1371/journal.pone.0308233

Figure Lengend Snippet: Effect of CXB and DMC combinations on ROS production (A) in HeLa and ROS content (B) in SiHa cells. Data shown represent the mean ± S.D. of at least three different preparations. *p < 0.05 vs . control (non-treated cells); **p < 0.05 vs . CXB or DMC.

Article Snippet: Human HeLa and SiHa cervix cancer cells were obtained from the ATCC (American Type Culture Collection).

Techniques: Control

Cell number (%) under apoptosis, determined by flux cytometry in HeLa (A) and SiHa (B) cells. (C) Contents of Caspase-1 and caspase-3 proteins. Data shown represent the mean ± S.D. of at least three different preparations. *p < 0.05 vs. control (non-treated cells). DOX, doxorubicin.

Journal: PLOS ONE

Article Title: Synergistic celecoxib and dimethyl-celecoxib combinations block cervix cancer growth through multiple mechanisms

doi: 10.1371/journal.pone.0308233

Figure Lengend Snippet: Cell number (%) under apoptosis, determined by flux cytometry in HeLa (A) and SiHa (B) cells. (C) Contents of Caspase-1 and caspase-3 proteins. Data shown represent the mean ± S.D. of at least three different preparations. *p < 0.05 vs. control (non-treated cells). DOX, doxorubicin.

Article Snippet: Human HeLa and SiHa cervix cancer cells were obtained from the ATCC (American Type Culture Collection).

Techniques: Cytometry, Control

Analytic sensitivity of HPV-seq. A, HPV-seq was conducted on fragmented SiHa genomic DNA at the indicated dilution. Hybrid capture baits targeted the indicated HPV-16 sequences. The lower limit of detection (LLOD) of HPV-seq was dependent on the use of dual-strand hybrid capture and the length of HPV-16 genome targeted by the baits. B, HPV-seq with full-length dual-strand hybrid capture (blue) provided an improvement in analytic sensitivity and LLOD (0.003%) as compared with hybrid capture for a single mutation (1%). C, Influence of multiple markers and sequencing depth on LLOD. Downsampling of HPV-seq data from full-length dual-strand hybrid capture demonstrates the dependence of the LLOD on the targeted length of HPV-16 genome (i.e., number of markers; right y -axis) and the sequencing depth ( x -axis). The probability of detecting the indicated number of HPV molecules (1, blue circles; 2, gray triangles; 5, yellow squares) is shown (left y -axis).

Journal: Clinical Cancer Research

Article Title: HPV Sequencing Facilitates Ultrasensitive Detection of HPV Circulating Tumor DNA

doi: 10.1158/1078-0432.CCR-19-2384

Figure Lengend Snippet: Analytic sensitivity of HPV-seq. A, HPV-seq was conducted on fragmented SiHa genomic DNA at the indicated dilution. Hybrid capture baits targeted the indicated HPV-16 sequences. The lower limit of detection (LLOD) of HPV-seq was dependent on the use of dual-strand hybrid capture and the length of HPV-16 genome targeted by the baits. B, HPV-seq with full-length dual-strand hybrid capture (blue) provided an improvement in analytic sensitivity and LLOD (0.003%) as compared with hybrid capture for a single mutation (1%). C, Influence of multiple markers and sequencing depth on LLOD. Downsampling of HPV-seq data from full-length dual-strand hybrid capture demonstrates the dependence of the LLOD on the targeted length of HPV-16 genome (i.e., number of markers; right y -axis) and the sequencing depth ( x -axis). The probability of detecting the indicated number of HPV molecules (1, blue circles; 2, gray triangles; 5, yellow squares) is shown (left y -axis).

Article Snippet: The SiHa cervix cancer cell line, which harbors 1 to 2 integrated copies of HPV-16 , was obtained from ATCC (catalog no. HTB-35, RRID:CVCL_0032).

Techniques: Mutagenesis, Sequencing

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