Journal: Translational Cancer Research

Article Title: Quetiapine inhibits the oxidative phosphorylation in head and neck squamous cell carcinoma through suppressing NAT10-mediated ac4C modification

doi: 10.21037/tcr-2025-1-2683

Figure Lengend Snippet: Quetiapine could regulate NAT10-mediated ac4C modification in HNSCC. (A) The mainly potential drugs identified by L1000FWD database. (B) The chemical structure of quetiapine. (C) Molecular docking of NAT10 and quetiapine. (D) The binding sensorgram of the interactions between NAT10 and quetiapine. (E) The protein expression of NAT10 was detected through western blotting (left) and quantitatively analyzed (right); n=3. From left to right, P=0.001, <0.001, and 0.002, respectively. (F) The mRNA expression of NAT10 in HNSCC cells; n=3. From left to right, P=0.03, 0.002, and 0.08, respectively. (G) The protein expression of NAT10 after SCC-15 cells were treated with quetiapine was detected through western blotting (left) and quantitatively analyzed (right); n=3. P<0.001. (H) The mRNA expression of NAT10 after SCC-15 cells were treated with quetiapine; n=3. P<0.001. (I) Dot blot assay was conducted to assess the ac4C level. P<0.001. Data are presented as mean ± SD. ns, no significance; *, P<0.05; **, P<0.01; ***, P<0.001 by unpaired t -test. EGFR, epidermal growth factor receptor; HDAC, histone deacetylase; HNSCC, head and neck squamous cell carcinoma; MEK, methyl ethyl ketone; MOA, mechanism of action; mRNA, messenger RNA; NF-κB, nuclear factor kappa-B; PARP, poly ADP-ribose polymerase; PLK, polo-like kinase; RAF, Raf kinase; RU, response unit; SD, standard deviation.

Article Snippet: The human oral keratinocytes (HOK) and three HNSCC cell lines, namely WSU-HN6, SCC-15 and CAL-27, were acquired from the American Type Culture Collection.

Techniques: Modification, Binding Assay, Expressing, Western Blot, Dot Blot, Histone Deacetylase Assay, Standard Deviation

Journal: Translational Cancer Research

Article Title: Quetiapine inhibits the oxidative phosphorylation in head and neck squamous cell carcinoma through suppressing NAT10-mediated ac4C modification

doi: 10.21037/tcr-2025-1-2683

Figure Lengend Snippet: Quetiapine treatment inhibited HNSCC malignant phenotypes in vitro . (A) CCK-8 assay showed that quetiapine treatment inhibited the proliferation of SCC-15 cells; n=5. P<0.001. (B) Representative images of SCC-15 clones treated with quetiapine using crystal violet solution staining. (C) The quantitation of colony number for SCC-15 cells treated with quetiapine; n=3. P=0.001. (D,E) Apoptosis assay results of SCC-15 cells treated with quetiapine; n=3. P=0.02. (F) Representative imaged of SCC-15 transwell migration treated with quetiapine using crystal violet solution staining. (G) Quantified of transwell migration in SCC-15 cells treated with quetiapine; n=3. P=0.003. (H,I) Wound healing assays showed the treatment of quetiapine inhibited migration of SCC-15 cells. The migration distance was quantified at 24 hours after scratching; n=3. P<0.001. *, P<0.05; **, P<0.01; ***, P<0.001 by unpaired t -test. CCK-8, Cell Counting Kit-8; FITC, fluorescein isothiocyanate; HNSCC, head and neck squamous cell carcinoma; PI, propidium iodide.

Article Snippet: The human oral keratinocytes (HOK) and three HNSCC cell lines, namely WSU-HN6, SCC-15 and CAL-27, were acquired from the American Type Culture Collection.

Techniques: In Vitro, CCK-8 Assay, Clone Assay, Staining, Quantitation Assay, Apoptosis Assay, Migration, Cell Counting

Journal: Translational Cancer Research

Article Title: Quetiapine inhibits the oxidative phosphorylation in head and neck squamous cell carcinoma through suppressing NAT10-mediated ac4C modification

doi: 10.21037/tcr-2025-1-2683

Figure Lengend Snippet: Quetiapine treatment inhibited the process of OXPHOS. (A) The mRNA expression of OXPHOS related genes after SCC-15 cells were treated with quetiapine; n=3. From left to right, P values <0.001, <0.001, <0.001, 0.02, <0.001, 0.003, 0.004, <0.001, and <0.001, respectively. (B) The protein expression of OXPHOS related proteins after SCC-15 cells were treated with quetiapine were detected through western blotting (left) and quantitatively analyzed (right); n=3. From left to right, P=0.002, <0.001, <0.001, 0.01, and 0.003, respectively. (C) OCR, which reflects mitochondrial respiration, was decreased in quetiapine treated SCC-15 cells. (D) Statistical chart of OCR various parameters about SCC-15 cells after treated with quetiapine; n=3. From left to right, P values <0.001, 0.002, 0.64, <0.001, and 0.07, respectively. ns, no significance; *, P<0.05, **, P<0.01; ***, P<0.005 by unpaired t -test. mRNA, messenger RNA; FCCP, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone; OCR, oxygen consumption rate; OXPHOS, oxidative phosphorylation.

Article Snippet: The human oral keratinocytes (HOK) and three HNSCC cell lines, namely WSU-HN6, SCC-15 and CAL-27, were acquired from the American Type Culture Collection.

Techniques: Expressing, Western Blot, Phospho-proteomics

Journal: Journal of Extracellular Vesicles

Article Title: VAMP4/STX8 Mediate the Autophagic Secretion of Mitochondria and Promote TAMs Polarization in HNSCC

doi: 10.1002/jev2.70276

Figure Lengend Snippet: Hypoxia led to abnormal mitochondrial morphology and function. (A) Immunofluorescence staining of mitochondrial morphology in HN6 cells. The cells were cultured under normoxia, hypoxia (48 h), or CCCP (2 h), and the mitochondria were labelled with HSP60. (B) Quantitative assessment of mitochondrial morphology in (A) using the Image J software. Five images per group were analysed randomly. (C) TEM images of the mitochondrial ultra‐structure in SCC25 and CAL27 cells under normoxia versus hypoxia. (D) JC‐1 aggregate/monomer ratios were measured by flow cytometry under normoxia, hypoxia, or CCCP treatment in CAL27 cells. (E) Quantification of mitochondrial depolarization. Median fluorescence intensity ratios of JC‐1 monomers versus aggregates were calculated and normalized against the mean values of the normoxia group. (F) MitoSOX assay to assess the mitochondrial superoxide levels in CAL27 cells. (G) Flow cytometric analysis of superoxide production after normoxia or hypoxia (48 h) treatment. (H) Seahorse extracellular flux assay under normoxia versus hypoxia in SCC25 cells. (I) Quantitative metrics of basal respiration, ATP production, maximal respiration, and spare capacity. (J) ATP production in CAL27 cells under hypoxia versus normoxia (48 h). Statistical analysis: Unpaired two‐tailed Student's t test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. The data are expressed as the mean ± standard deviations (SD).

Article Snippet: The SCC25 and CAL27 cell lines were obtained from ATCC (USA), and the UMD School of Dentistry (USA) provided the HN6 cell line.

Techniques: Immunofluorescence, Staining, Cell Culture, Software, Flow Cytometry, Fluorescence, Mitosox Assay, XF Assay, Two Tailed Test

Journal: Journal of Extracellular Vesicles

Article Title: VAMP4/STX8 Mediate the Autophagic Secretion of Mitochondria and Promote TAMs Polarization in HNSCC

doi: 10.1002/jev2.70276

Figure Lengend Snippet: Hypoxia caused mitophagy, which does not involve fusion with lysosomes. (A) Spatial clustering of heterogeneous mitophagy and hypoxia profiles was observed across tumour and adjacent tissues in 10× Visium spatial transcriptomic slides. (B) Western blot analysis of the expression levels of PINK1, P62, LC3B, and p‐Ub. Proteins were extracted from SCC25 cells subjected to normoxia, hypoxia, or lactic acid for 48 h; starvation for 12 h; or CCCP treatment for 2 h. (C) Immunofluorescence staining of HN6 cells using MitoTracker and LC3B. (D) Quantitative analysis of LC3B‐MitoTracker co‐localization in (C), with n = 10 cells per group. (E) TEM images of the mitochondrial autophagosomes in SCC25 and CAL27 cells. (F) Quantification of mitochondrial autophagosomes per cell in (E), analysed in n = 10 cells per group. (G) HN6 cells subjected to normoxia, hypoxia (48 h), or CCCP (2 h) were stained with MitoTracker and LAMP1 to assess the degree of mitochondrial–lysosomal fusion. Statistical analysis: Unpaired two‐tailed Student's t test. **** p < 0.0001. The data are expressed as the mean ± SD.

Article Snippet: The SCC25 and CAL27 cell lines were obtained from ATCC (USA), and the UMD School of Dentistry (USA) provided the HN6 cell line.

Techniques: Western Blot, Expressing, Immunofluorescence, Staining, Two Tailed Test

Journal: Journal of Extracellular Vesicles

Article Title: VAMP4/STX8 Mediate the Autophagic Secretion of Mitochondria and Promote TAMs Polarization in HNSCC

doi: 10.1002/jev2.70276

Figure Lengend Snippet: Hypoxia damaged lysosomal homeostasis. (A) Schematic illustration of mitochondrial autophagosome‒lysosome fusion and degradation. (B) Western blot analysis of the expression levels of LAMP1 and CTSD. Proteins were extracted from SCC25 and CAL27 cells subjected to normoxia and hypoxia for 48 h. (C) Representative TEM images of lysosomes from SCC25 and CAL27 cells subjected to hypoxia and normoxia. (D) Confocal microscopy analysis of LAMP1 in HN6 cells. (E) Lysosomal diameter distribution from three independent experiments ( n > 80 in each group). (F) The frequency distribution of lysosomal diameters indicated that the number of lysosomes (diameter < 800 nm) in hypoxic cells decreased, whereas the number of large lysosomes (diameter > 800 nm) increased significantly. (G) LysoTracker Red assay of HN6 cells exposed to normoxia or hypoxia for 48 h. (H) Quantification of the number of LysoTracker‐positive points in Figure G. Ten fields were randomly selected from each group for analysis. (I) Lysosomal pH was determined using Lysosensor yellow/blue DND‐160. Each point represents the lysosomal pH from an independent experiment. (J) Co‐localization of LAMP1 and TOM70 in HN6 cells. Statistical analysis was performed using an unpaired two‐tailed Student's t test. ** p < 0.01, **** p < 0.0001. The data are expressed as the mean ± SD.

Article Snippet: The SCC25 and CAL27 cell lines were obtained from ATCC (USA), and the UMD School of Dentistry (USA) provided the HN6 cell line.

Techniques: Western Blot, Expressing, Confocal Microscopy, Two Tailed Test

Journal: Journal of Extracellular Vesicles

Article Title: VAMP4/STX8 Mediate the Autophagic Secretion of Mitochondria and Promote TAMs Polarization in HNSCC

doi: 10.1002/jev2.70276

Figure Lengend Snippet: Hypoxia promoted the release of mitochondrial components through EV. (A) Co‐localization of RAB27A and TOM70 in HN6 cells under normoxia or hypoxia for 48 h. Co‐localization levels were quantified using the ImageJ software. (B) Fluorescence co‐localization of CD81 and HSP60 in HN6 cells after 48 h of normoxia/hypoxia. (C) HSP60 and CD81 co‐localization levels in hypoxic regions of HNSCC samples determined by multiplex immunohistochemistry (mIHC) staining. The images represent distinct regions in the same patient. (D) Mitochondrial proteins were significantly enriched in EV, as analysed by gene ontology (GO) enrichment. (E) Heatmap depicting mitochondria‐related differentially expressed proteins in EV under normoxic and hypoxic conditions. (F) Proportion of mitochondrial and non‐mitochondrial proteins in the EV. (G) Western blot analysis of EV purified from SCC25 cell culture supernatant. The mitochondrial proteins COXIV, ACO2, HSP60, and CS were detected, with ALIX serving as an EV loading control. (H) qPCR quantification of mtDNA in EV. Statistical analysis: unpaired two‐tailed Student's t test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. The data are presented as the mean ± SD.

Article Snippet: The SCC25 and CAL27 cell lines were obtained from ATCC (USA), and the UMD School of Dentistry (USA) provided the HN6 cell line.

Techniques: Software, Fluorescence, Multiplex Assay, Immunohistochemistry, Staining, Western Blot, Purification, Cell Culture, Control, Two Tailed Test

Journal: Journal of Extracellular Vesicles

Article Title: VAMP4/STX8 Mediate the Autophagic Secretion of Mitochondria and Promote TAMs Polarization in HNSCC

doi: 10.1002/jev2.70276

Figure Lengend Snippet: ATP6V1A overexpression led to a decrease in mitochondrial components in EV. (A) HN6 cells overexpressing ATP6V1A were exposed to hypoxia for 48 h and co‐stained with LAMP1 and HSP60. (B) Fluorescence co‐localization of CD81 and HSP60 in ATP6V1A‐overexpressing HN6 cells after 48 h of hypoxia. (C) EV from SCC25 cell supernatants (hypoxia‐treated and ATP6V1A‐overexpressing cells) were analysed by western blot. Mitochondrial proteins (COXIV, ACO2, HSP60, and CS) were detected, with ALIX serving as a loading control. (D) qPCR quantification of mtDNA in EV. (E) Western blot analysis of EV purified from HN6, SCC25, and CAL27 cells under normoxic or hypoxic conditions. Syntenin was used as a loading control. (F) HN6 cells with LC3B knockdown were stained with MitoTracker to visualize mitochondrial morphology. (G) EV purified from SCC25 cell supernatants (hypoxia‐treated, LC3B‐knockdown) were analysed by western blot. Mitochondrial proteins (TOM70, COXIV, and CS) were detected using syntenin as the loading control. (H) qPCR quantification of mtDNA in EV. Statistical analysis: Unpaired two‐tailed Student's t test. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. The data are presented as the mean ± SD.

Article Snippet: The SCC25 and CAL27 cell lines were obtained from ATCC (USA), and the UMD School of Dentistry (USA) provided the HN6 cell line.

Techniques: Over Expression, Staining, Fluorescence, Western Blot, Control, Purification, Knockdown, Two Tailed Test

Journal: Journal of Extracellular Vesicles

Article Title: VAMP4/STX8 Mediate the Autophagic Secretion of Mitochondria and Promote TAMs Polarization in HNSCC

doi: 10.1002/jev2.70276

Figure Lengend Snippet: The vesicle transporter proteins VAMP4 and STX8 mediated ASM. (A) Schematic representation of MVB isolation via density gradient sucrose centrifugation. (B) KEGG pathway enrichment analysis of differentially expressed proteins among MVB members. (C) The predicted interaction model of VAMP4 and STX8 visualized using PyMOL. The red regions denote the interface‐binding domains. (D) Co‐immunoprecipitation (co‐IP) assays confirmed the VAMP4‐STX8 interaction in HN6 and CAL27 cells. (E) Co‐IP analysis confirmed VAMP4‐STX8 complex formation within MVB isolated from HN6 and CAL27 cells. (F) Immunofluorescence staining for VAMP4, STX8, and CD63 in HN6 cells. (G) Immunofluorescence staining for VAMP4, STX8, CD81, and LC3B in HN6 cells. (H) Western blot analysis of VAMP4 and STX8 expression in HN6 and CAL27 cells under normoxia and hypoxia (0–48 h). (I) Hypoxia‐treated HN6 cells transfected with siVAMP4/siSTX8 were subjected to mIHC for HSP60, LC3B, and CD81 co‐localization. (J) Western blot quantification of mitochondrial proteins (COXIV and HSP60) in EV purified from SCC25 cells under hypoxia/normoxia with siVAMP4/siSTX8 knockdown. ALIX was used as the loading control. (K) qPCR quantification of mtDNA in EV isolated from SCC25 cells. (L) Western blot analysis of apoptosis‐related proteins (Bax and Caspase‐9) in SCC25 cells subjected to hypoxia/normoxia with mitophagy inhibition (3MA) or siVAMP4/siSTX8 transfection. (M) Western blot analysis of mitochondrial proteins (COXIV, ACO2, HSP60, and CS) in EV from HN6 cells transfected with VAMP4/STX8 truncation plasmids under hypoxia. ALIX was used as the loading control. (N, O) RT‐qPCR quantification of mtDNA in EV from HN6 cells transfected with VAMP4/STX8 truncation plasmids. Statistical analysis: unpaired two‐tailed Student's t test; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. The data are presented as the mean ± SD.

Article Snippet: The SCC25 and CAL27 cell lines were obtained from ATCC (USA), and the UMD School of Dentistry (USA) provided the HN6 cell line.

Techniques: Isolation, Centrifugation, Binding Assay, Immunoprecipitation, Co-Immunoprecipitation Assay, Immunofluorescence, Staining, Western Blot, Expressing, Transfection, Purification, Knockdown, Control, Inhibition, Quantitative RT-PCR, Two Tailed Test

Journal: Journal of Extracellular Vesicles

Article Title: VAMP4/STX8 Mediate the Autophagic Secretion of Mitochondria and Promote TAMs Polarization in HNSCC

doi: 10.1002/jev2.70276

Figure Lengend Snippet: STX4 and SNAP23 mediate EV release. (A) mIHC analysis of VAMP4, STX4, SNAP23, and CD81 co‐localization in hypoxia‐treated HN6 cells. TEM images of EV (B) and MVB (C) isolated from HN6 cells transfected with siSTX4 or siSNAP23. (D) NTA of EV size and quantity in SCC25 cells transfected with siSTX4/siSNAP23. EV were isolated from 2 × 10 6 cells/group. (E) BCA assay quantification of protein concentrations in EV collected from equal numbers of cells. (F) Western blot analysis of EV markers (ALIX, TSG101, and RAB5) in CAL27 cells transfected with siSTX4/siSNAP23. (G) Hypoxia‐treated SCC25 cells were transfected with siSTX4/siSNAP23. Western blot analysis of mitochondrial proteins (ACO2 and HSP60) in EV. ALIX was used as the loading control. (H) qPCR quantification of mtDNA in EV derived from CAL27 cells transfected with siSTX4/siSNAP23. (I) A schematic diagram of proposed mechanism. Statistical analysis: unpaired two‐tailed Student's t test; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. The data are presented as the mean ± SD.

Article Snippet: The SCC25 and CAL27 cell lines were obtained from ATCC (USA), and the UMD School of Dentistry (USA) provided the HN6 cell line.

Techniques: Isolation, Transfection, BIA-KA, Western Blot, Control, Derivative Assay, Two Tailed Test

Journal: Radiation Oncology (London, England)

Article Title: CXCR2 affects sensitization of radioresistant HPV-negative head and neck squamous cell carcinoma cells by ABT-263

doi: 10.1186/s13014-026-02798-w

Figure Lengend Snippet: ABT-263 induces cell death by inhibiting anti-apoptotic and increasing pro-apoptotic proteins. Cells were treated with 1–7 µM ABT-263 and 6 Gy irradiation. ( A ) Cal33 ( N = 2) and ( B ) UPCI:SCC040 ( N = 4). AnnexinV assays were performed to assess viable, early apoptotic and late apoptotic/necrotic cells 4 days after treatment. Values represent means ± SEM of N replicates. Statistical significance was determined using Student’s t test, p < 0.05 (*). ( C ) Cal33 and ( D ) UPCI:SCC040 protein lysates were analyzed 4 (D4) or 6 (D6) days after treatment. Representative Western blots and densitometric quantification ( N = 2) are shown for pro-Caspase-9, Bcl-xL and Bax. Stauro = staurosporine

Article Snippet: HPV-negative HNSCC cell lines UPCI:SCC040 and Cal33 were purchased from DSMZ (RRID:CVCL_2222 and CVCL 1108, DSMZ, Germany Cat#ACC660 and Cat#ACC447).

Techniques: Irradiation, Western Blot

Journal: Radiation Oncology (London, England)

Article Title: CXCR2 affects sensitization of radioresistant HPV-negative head and neck squamous cell carcinoma cells by ABT-263

doi: 10.1186/s13014-026-02798-w

Figure Lengend Snippet: ABT-263 decreases senescence in Cal33 and UPCI:SCC040 cells. Cells were treated with 1–6 µM ABT-263 and 6 Gy irradiation and analyzed on day 4 (D4) or day 6 (D6). ( A ) Representative images of UPCI:SCC040 cells treated with 5 µM ABT-263, 6 Gy irradiation, and controls. Morphology is shown for adherent viable cells (orange), proliferating mitotic cells (green), apoptotic cells (blue), senescent cells (yellow) and degraded debris (red). ( B ) Flow-cytometric analysis of senescence-associated β-galactosidase–positive cells in Cal33 (left panel) and UPCI:SCC040 (right panel). Values represent means ± SEM of N ≥ 3 replicates. Student´s t test: p < 0.05 (*), p < 0.01 (**). ( C-D ) Lamin B1 detection by Western Blot with densitometric quantification ( N = 2)

Article Snippet: HPV-negative HNSCC cell lines UPCI:SCC040 and Cal33 were purchased from DSMZ (RRID:CVCL_2222 and CVCL 1108, DSMZ, Germany Cat#ACC660 and Cat#ACC447).

Techniques: Irradiation, Western Blot

Journal: Radiation Oncology (London, England)

Article Title: CXCR2 affects sensitization of radioresistant HPV-negative head and neck squamous cell carcinoma cells by ABT-263

doi: 10.1186/s13014-026-02798-w

Figure Lengend Snippet: ABT-263 affects viability and clonogenic survival of HPV-negative HNSCC cells. Alamar blue assays were performed on day 6 (D6) after treatment with 6 Gy irradiation and various ABT-263 concentrations for ( A ) UPCI:SCC040 and ( B ) Cal33. Values were normalized to DMSO controls. Plating efficiency was assessed via colony formation assays in ( C ) Cal33 and ( D ) UPCI:SCC040 cells treated with ABT-263. ( E ) Representative colony formation images after irradiation and ABT-263 treatment. ( F,G ) Colony formation assay after 2, 4 and 6 Gy irradiation. ( F ) Cal33 treated with 1 µM ABT-263. ( G ) UPCI:SCC040 treated with 5 or 6 µM ABT-263. DMSO served as control. Values represent means ± SEM of N ≥ 3 replicates. Student´s t test: p < 0.05 (*), p < 0.01 (**), ns: not significant

Article Snippet: HPV-negative HNSCC cell lines UPCI:SCC040 and Cal33 were purchased from DSMZ (RRID:CVCL_2222 and CVCL 1108, DSMZ, Germany Cat#ACC660 and Cat#ACC447).

Techniques: Irradiation, Colony Assay, Control

Journal: Radiation Oncology (London, England)

Article Title: CXCR2 affects sensitization of radioresistant HPV-negative head and neck squamous cell carcinoma cells by ABT-263

doi: 10.1186/s13014-026-02798-w

Figure Lengend Snippet: ABT-263 decreases senescence and alters the SASP in UPCI:SCC040 and Cal33 cells. Cells were treated with 1 µM ABT-263 (Cal33) or 5 µM of ABT-263 (UPCI:SCC040) concomitantly with 6 Gy irradiation and analyzed on D4 or D6. ( A-B ) Gene expression of secreted factors measured by qRT-PCR and normalized to unirradiated DMSO controls. ( A ) UPCI:SCC040. ( B ) Cal33. ( C-D ) Secreted IL1A, IL1B, IL8 and CXCL1 protein levels were detected by ELISA on D4 and D6. Protein concentrations (pg/ml) were normalized to cell number. ( C ) UPCI:SCC040. ( D ) Cal33. ( E-F ) Relative CXCR2 gene expression shown as ΔCT values in ( E ) Cal33 and ( F ) UPCI:SCC040 cells. Values a represent means ± SEM of N = 2. Student’s t test: p < 0.05 (*), p < 0.01 (**), ns: not significant

Article Snippet: HPV-negative HNSCC cell lines UPCI:SCC040 and Cal33 were purchased from DSMZ (RRID:CVCL_2222 and CVCL 1108, DSMZ, Germany Cat#ACC660 and Cat#ACC447).

Techniques: Irradiation, Gene Expression, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

Journal: Radiation Oncology (London, England)

Article Title: CXCR2 affects sensitization of radioresistant HPV-negative head and neck squamous cell carcinoma cells by ABT-263

doi: 10.1186/s13014-026-02798-w

Figure Lengend Snippet: CXCR2 knockdown (KD) in combination with ABT-263 treatment radiosensitizes UPCI:SCC040 cells. ( A ) Time-course analysis of CXCR2 KD, validated by qRT-PCR 6 days after transfection. Expression was normalized to the siNont control. ( B ) Plating efficiency was assessed by colony formation. Cells were reseeded 24 h after transfection and treated with 1 µM ABT-263 after adhesion. DMSO served as control. ( C-D ) Colony formation after 2, 4 and 6 Gy irradiation. ( C ) Survival curves of untreated UPCI:SCC040 siNont vs. siCXCR2 KD. ( D-E ) Survival curves of ( D ) siNont and ( E ) siCXCR2 cells with 1 µM ABT-263 immediately prior to irradiation. Values are are means ± SEM of N ≥ 3 replicates. Student’s t test: p < 0.05 (*), p < 0.01 (**), ns: not significant

Article Snippet: HPV-negative HNSCC cell lines UPCI:SCC040 and Cal33 were purchased from DSMZ (RRID:CVCL_2222 and CVCL 1108, DSMZ, Germany Cat#ACC660 and Cat#ACC447).

Techniques: Knockdown, Quantitative RT-PCR, Transfection, Expressing, Control, Irradiation

Journal: Radiation Oncology (London, England)

Article Title: CXCR2 affects sensitization of radioresistant HPV-negative head and neck squamous cell carcinoma cells by ABT-263

doi: 10.1186/s13014-026-02798-w

Figure Lengend Snippet: siCXCR2 KD does not alter DSB repair foci after ABT-263 treatment and 1 Gy irradiation. ( A ) Representative images of DSBs in Cal33 (left) and UPCI:SCC040 (right). Nuclei were stained with DAPI (blue); residual DSBs at 24 h post-irradiation were visualized by γH2AX (red) and 53BP1 (green). ( B ) Residual DSB foci in Cal33 cells treated with 1 µM ABT-263 before irradiation. DMSO served as control. ( C ) Residual DSB foci in transfected UPCI:SCC040 cells treated with 1 µM ABT-263 before irradiation, comparing siCXCR2 with siNont. Values represent means ± SEM of N ≥ 3 replicates, background foci were subtracted. Student’s t test: p < 0.05 (*), p < 0.01 (**), ns: not significant

Article Snippet: HPV-negative HNSCC cell lines UPCI:SCC040 and Cal33 were purchased from DSMZ (RRID:CVCL_2222 and CVCL 1108, DSMZ, Germany Cat#ACC660 and Cat#ACC447).

Techniques: Irradiation, Staining, Control, Transfection