caski human cervical carcinoma cells  (Korean Cell Line Bank)

Journal: Medicina

Article Title: Expression of Core Hippo Pathway Proteins in Cervical Cancer and Their Association with Clinicopathologic Parameters

doi: 10.3390/medicina61122134

Figure Lengend Snippet: YAP knockdown efficiency confirmed by RT-PCR in Caski cervical cancer cells. ( A ) Representative RT-PCR images from four independent experiments (#1–#4), demonstrating consistently reduced YAP mRNA expression in YAP-silenced (K.D) cells compared with negative control (N.C) cells. GAPDH served as the internal control and exhibited stable expression. Full-length, uncropped gels are provided in . ( B ) Relative YAP mRNA expression normalized to GAPDH, based on densitometric analysis using ImageJ. Data represent the mean ± SD from four independent experiments. YAP expression decreased by approximately 50% in the K.D group (*** p < 0.001).

Article Snippet: Caski human cervical carcinoma cells were obtained from the Korean Cell Line Bank and cultured in RPMI-1640 medium (Gibco, Thermo Fisher Scientific, Waltham, MA, USA) supplemented with 10% fetal bovine serum and 1% penicillin–streptomycin at 37 °C in a humidified atmosphere containing 5% CO 2 .

Techniques: Knockdown, Reverse Transcription Polymerase Chain Reaction, Expressing, Negative Control, Control

Journal: Medicina

Article Title: Expression of Core Hippo Pathway Proteins in Cervical Cancer and Their Association with Clinicopathologic Parameters

doi: 10.3390/medicina61122134

Figure Lengend Snippet: Western blot validation of YAP knockdown in Caski cervical cancer cells. ( A ) Representative blots from four independent experiments showing reduced YAP and P-YAP expression in the knockdown (K.D) group compared with the negative control (N.C), with GAPDH as the loading control. ( B ) Densitometric analysis demonstrating an approximately 50% decrease in YAP levels in the K.D group (*** p < 0.001). ( C ) Densitometric analysis showing an approximately 45% reduction in P-YAP levels in the K.D group (** p < 0.01). Data represent mean ± SD from four experiments.

Article Snippet: Caski human cervical carcinoma cells were obtained from the Korean Cell Line Bank and cultured in RPMI-1640 medium (Gibco, Thermo Fisher Scientific, Waltham, MA, USA) supplemented with 10% fetal bovine serum and 1% penicillin–streptomycin at 37 °C in a humidified atmosphere containing 5% CO 2 .

Techniques: Western Blot, Biomarker Discovery, Knockdown, Expressing, Negative Control, Control

Journal: Medicina

Article Title: Expression of Core Hippo Pathway Proteins in Cervical Cancer and Their Association with Clinicopathologic Parameters

doi: 10.3390/medicina61122134

Figure Lengend Snippet: Wound-healing assay demonstrating the effect of YAP knockdown on cell migration in Caski cervical cancer cells. ( A ) Representative wound-healing images of negative control (N.C) and YAP-silenced (K.D) cells captured at 0, 12, 24, and 48 h after scratch formation. Red dashed lines indicate the original wound boundaries. YAP-silenced cells demonstrated visibly slower wound closure compared with N.C cells. ( B ) Quantitative measurement of wound gap distance using ImageJ. Gap width was measured across three independent experiments, and values are presented as mean ± SD. Significant differences between groups were observed at 24 h and 48 h ( p < 0.01), indicating impaired migratory ability following YAP suppression.

Article Snippet: Caski human cervical carcinoma cells were obtained from the Korean Cell Line Bank and cultured in RPMI-1640 medium (Gibco, Thermo Fisher Scientific, Waltham, MA, USA) supplemented with 10% fetal bovine serum and 1% penicillin–streptomycin at 37 °C in a humidified atmosphere containing 5% CO 2 .

Techniques: Wound Healing Assay, Knockdown, Migration, Negative Control

Journal: Cancers

Article Title: DHODH Inhibition Exerts Synergistic Therapeutic Effect with Cisplatin to Induce Ferroptosis in Cervical Cancer through Regulating mTOR Pathway

doi: 10.3390/cancers15020546

Figure Lengend Snippet: Inhibition of DHODH suppresses cell proliferation and promotes cell death in cervical cancer cells. ( A ) The expression level of DHODH protein in human cervical cancer tissues and adjacent non-tumor tissues was measured by IHC staining. Scale bar = 100 μm. IHC scores were used to analyze the experimental results. *** p < 0.001 compared to the normal tissues. ( B ) The efficacy of DHODH knockdown in CaSki and HeLa cells was measured by Western blotting. The relative expression of DHODH was calculated by ImageJ software in each group ( n = 3). ** p < 0.01, *** p < 0.001 compared to the control group. ( C ) The effect of DHODH knockdown on cell viability was measured by CCK-8 assays in cervical cancer cells. *** p < 0.001 compared to the control group. ( D ) The effect of DHODH knockdown on clonogenicity was measured by the colony formation assay in cervical cancer cells. ( E ) Sensitivity to brequinar (BQR) was assessed using the CCK-8 assay in CaSki and HeLa cells treated with BQR (0, 0.01, 0.1, 1, 10, 100 μM) for 24, 48 and 72 h. ( F ) The effect of BQR (0.7 μM for CaSki cells; 0.3 μM for HeLa cells) on cell death was assessed by the flow cytometry analysis through PI staining. *** p < 0.001 compared to the control group.

Article Snippet: Human cervical adenocarcinoma HeLa cells and human cervical squamous cell carcinoma CaSki cells were provided from ATCC (Manassas, VA, USA).

Techniques: Inhibition, Expressing, Immunohistochemistry, Knockdown, Western Blot, Software, Control, CCK-8 Assay, Colony Assay, Flow Cytometry, Staining

Journal: Cancers

Article Title: DHODH Inhibition Exerts Synergistic Therapeutic Effect with Cisplatin to Induce Ferroptosis in Cervical Cancer through Regulating mTOR Pathway

doi: 10.3390/cancers15020546

Figure Lengend Snippet: Inhibition of DHODH induces ferroptotic cell death in cervical cancer cells. ( A ) The effect of DHODH knockdown on lipid peroxidation in CaSki and HeLa cells was measured by MDA level detection. ** p < 0.01, *** p < 0.001 compared to the control group. ( B ) The effect of brequinar (BQR) on lipid peroxidation in CaSki (2 μM) and HeLa (1 μM) cells was measured by MDA level detection after treated for 48 h. *** p < 0.001 compared to the control group. ( C ) Cell viability of CaSki and HeLa cells treated with BQR (0.7 μM for CaSki cells; 0.3 μM for HeLa cells) and/or liproxstatin-1 (Lip-1) (2 μM) for 24 h was measured by CCK-8 assays. * p < 0.05, ** p < 0.01, *** p < 0.001. ( D ) The lipid peroxidation of CaSki and HeLa cells treated with BQR (0.7 μM for CaSki cells; 0.3 μM for HeLa cells) and/or Lip-1 (2 μM) for 24 h was measured by MDA level detection. ** p < 0.01, *** p < 0.001. ( E ) The mitochondrial dysfunction in CaSki and HeLa cells treated with or without BQR (0.7 μM for CaSki cells; 0.3 μM for HeLa cells) was measured by mitochondrial membrane potential detection through JC-1 staining. Scale bar = 100 μm. *** p < 0.001 compared to the control group.

Article Snippet: Human cervical adenocarcinoma HeLa cells and human cervical squamous cell carcinoma CaSki cells were provided from ATCC (Manassas, VA, USA).

Techniques: Inhibition, Knockdown, Control, CCK-8 Assay, Membrane, Staining

Journal: Cancers

Article Title: DHODH Inhibition Exerts Synergistic Therapeutic Effect with Cisplatin to Induce Ferroptosis in Cervical Cancer through Regulating mTOR Pathway

doi: 10.3390/cancers15020546

Figure Lengend Snippet: Brequinar (BQR) synergizes with cisplatin (DDP) to exert anticancer effects by inducing ferroptotic death in cervical cancer cells in vitro. ( A ) Cell viability of CaSki and HeLa cells treated with BQR (0.2 μM for CaSki cells; 0.1 μM for HeLa cells) and/or DDP (2 μM for CaSki cells; 1 μM for HeLa cells) for 48 h was measured by CCK-8 assays. ** p < 0.01, *** p < 0.001 compared to the control group. ( B ) The synergistic effect of BQR (0.2 μM for CaSki cells; 0.1 μM for HeLa cells) and DDP (2 μM for CaSki cells; 1 μM for HeLa cells) was measured in CaSki and HeLa cells. ( C ) The effect of combination of BQR (0.2 μM for CaSki cells; 0.1 μM for HeLa cells) and DDP (2 μM for CaSki cells; 1 μM for HeLa cells) on cell death in cervical cancer cells was assessed by flow cytometry analysis through PI staining. *** p < 0.001. ( D ) The mitochondrial dysfunction in CaSki and HeLa cells treated with BQR (0.2 μM for CaSki cells; 0.1 μM for HeLa cells) and/or DDP (2 μM for CaSki cells; 1 μM for HeLa cells) was measured by mitochondrial membrane potential detection through JC-1 staining. *** p < 0.001. ( E ) The synergistic effect of DHODH inhibition ( DHODH knockdown or BQR (0.2 μM for CaSki cells; 0.1 μM for HeLa cells)) and DDP (2 μM for CaSki cells; 1 μM for HeLa cells) on lipid peroxidation was measured by MDA level detection in cervical cancer cells. * p < 0.05, *** p < 0.001.

Article Snippet: Human cervical adenocarcinoma HeLa cells and human cervical squamous cell carcinoma CaSki cells were provided from ATCC (Manassas, VA, USA).

Techniques: In Vitro, CCK-8 Assay, Control, Flow Cytometry, Staining, Membrane, Inhibition, Knockdown

Journal: Cancers

Article Title: DHODH Inhibition Exerts Synergistic Therapeutic Effect with Cisplatin to Induce Ferroptosis in Cervical Cancer through Regulating mTOR Pathway

doi: 10.3390/cancers15020546

Figure Lengend Snippet: Brequinar (BQR) synergizes with cisplatin (DDP) to suppress the expression of DHODH via inhibiting mTOR pathway. ( A ) The levels of DHODH, p-mTOR and mTOR proteins were detected by Western blotting in CaSki and HeLa cells treated with BQR (0.2 μM for CaSki cells; 0.1 μM for HeLa cells) and/or DDP (2 μM for CaSki cells; 1 μM for HeLa cells) for 48 h. ( B – D ) Relative expression of DHODH, p-mTOR, and mTOR was calculated by ImageJ software in each group ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Human cervical adenocarcinoma HeLa cells and human cervical squamous cell carcinoma CaSki cells were provided from ATCC (Manassas, VA, USA).

Techniques: Expressing, Western Blot, Software

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-29a Manifests Multifaceted Features to Intensify Radiosensitivity, Escalate Apoptosis, and Revoke Cell Migration for Palliating Radioresistance-Enhanced Cervical Cancer Progression

doi: 10.3390/ijms23105524

Figure Lengend Snippet: Suppressed miR-29a but not miR-29b/c in radioresistant (RR: 6 months) clones and their parental wild-type (WT) clones generated from CaSki and C33A cervical cancer cells. ( A ) Expression levels of miR-29a/b/c in WT and RR cervical cancer cells (CaSki) and ( B ) C33A cells. Cells were cultivated, collected, and the total microRNA was extracted, and expression levels of miR-29a , miR-29b, or miR-29c were estimated by quantitative RT-PCR analysis. The results were from two independent clones of CaSki and C33A cells, and each clone was repeated at least three times, and the results were similar. Data were shown as mean ± SD. ** p < 0.01, *** p < 0.001 for RR group vs. WT group.

Article Snippet: Human cervical carcinoma cell lines CaSki and C33A were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Clone Assay, Generated, Expressing, Quantitative RT-PCR

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-29a Manifests Multifaceted Features to Intensify Radiosensitivity, Escalate Apoptosis, and Revoke Cell Migration for Palliating Radioresistance-Enhanced Cervical Cancer Progression

doi: 10.3390/ijms23105524

Figure Lengend Snippet: Radiation survival curve of CaSki and C33A cells performed on cells in log phase growth to evaluate the radiosensitivity. Wild-type (WT) cells were transfected with Scrambled NC (100 nM) or miR-29a antisense (also termed miR-29a AS; 100 nM) , whereas the radioresistant (RR) cells were transfected with Scrambled NC (100 nM) or Pre miR-29a precursor (also termed Pre miR-29a; 100 nM), respectively. Cells were plated, irradiated, and assayed for clonogenic survival at the designated dosages. All of the clonogenic assays were repeated at least three times, as described in . The survival curve showed the reduced radiosensitivity of the stable radioresistant clones of ( A ) CaSki and ( B ) C33A cells to irradiation compared to their parental wild-type cells. RR-cells transfected with Pre miR-29a reduced the surviving fraction (elevated radiosensitivity), while WT-cells transfected with miR-29a AS enhanced the surviving fraction (decreased radiosensitivity). Shown are mean values, and error bars show the standard deviation (SD). Solid and dotted curves represent WT and RR cells, respectively. Filled circles, WT-Scrambled NC; open circles, RR-Scrambled NC. Filled squares, WT- miR-29a AS ; open squares, RR- Pre miR-29a . Each experiment was performed in triplicate and the results were similar.

Article Snippet: Human cervical carcinoma cell lines CaSki and C33A were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Transfection, Irradiation, Clone Assay, Standard Deviation

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-29a Manifests Multifaceted Features to Intensify Radiosensitivity, Escalate Apoptosis, and Revoke Cell Migration for Palliating Radioresistance-Enhanced Cervical Cancer Progression

doi: 10.3390/ijms23105524

Figure Lengend Snippet: Suppressed apoptosis rate was exhibited in radioresistant CaSki and C33A cells, and overexpression of m icroRNA-29a triggered the apoptosis in radioresistant cervical cancer cells. ( A ) Representative figure of flow cytometric analysis Annexin-V/PI double staining was executed on WT- or RR-CaSki cells, which were pre-transfected with Scramble NC, miR-29a AS, or Pre-miR29a , and then were subjected to the 6-Gy radiation treatment and the apoptosis rate was estimated, as described in . Summary of apoptotic cells (sum of Annexin-V-positive/PI-negative and Annexin-V-positive/PI-positive cells) over 48 h after 6-Gy radiation treatment. ( B ) CaSki cells or ( C ) C33A cells. Data were obtained from three independent experiments in triplicate and shown as the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Human cervical carcinoma cell lines CaSki and C33A were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Over Expression, Double Staining, Transfection

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-29a Manifests Multifaceted Features to Intensify Radiosensitivity, Escalate Apoptosis, and Revoke Cell Migration for Palliating Radioresistance-Enhanced Cervical Cancer Progression

doi: 10.3390/ijms23105524

Figure Lengend Snippet: Radioresistant (RR) CaSki and C33A cells exhibited augmented migration in vitro, and overexpression of miR-29a effectively abrogated RR-augmented cell migration. ( A ) Representative phase-contrast micrographs depicting scratched monolayers of serum-starved WT and RR CaSki and C33A cells at 0 and 8 h. Scale bar = 100 μm. The results of each cell were repeated at least three times, and the results were similar. ( B ) Summary of wound healing 8 h after scratching. Data are shown as mean ± SD. ( C ) Representative cell migration trace from a time-lapse recording of cell migration over 8 h. The results are representative of C33A and CaSki cell clones, and each clone was repeated at least three times. Scale bar = 100 μm. ( D ) Summary of migration speed from a time-lapse recording of cell migration over 8 h. Data are the mean ± SD of three independent experiments. All radioresistant C33A and CaSki cell clones underwent stable selection for 6 months after irradiation, and >20 cells per individual sample were counted. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Human cervical carcinoma cell lines CaSki and C33A were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Migration, In Vitro, Over Expression, Clone Assay, Selection, Irradiation

Journal: Marine Drugs

Article Title: RSK1 vs. RSK2 Inhibitory Activity of the Marine β-Carboline Alkaloid Manzamine A: A Biochemical, Cervical Cancer Protein Expression, and Computational Study

doi: 10.3390/md19090506

Figure Lengend Snippet: SiHa and CaSki human cervical carcinoma cells were treated with 2 and 4 µM of MZA for 48 h and protein expression of RSK1 and RSK2 was determined by Western blot assay. ( A ) Representative blots of RSK1 and RSK2 expression, ( B ) histograms from the pooled data for RSK1 and RSK2 repeats ( n = 3), and ( C ) the use of higher concentration of MZA (4 and 6 µM) for 48 h and its effect on phospho-RSK inhibition. Data represented as mean ± SE of three independent experiments; * p < 0.05 and ** p < 0.01; ns = non-specific.

Article Snippet: SiHa and CaSki human cervical carcinoma cell lines were obtained from ATCC and maintained as described previously [ ].

Techniques: Expressing, Western Blot, Concentration Assay, Inhibition