Journal: Journal of Cell Science

Article Title: Interplay between nuclear survivin and the PRC2 complex and its impact on H3K27me3-directed transcriptional repression

doi: 10.1242/jcs.264572

Figure Lengend Snippet: Hypoxia increases expression of EZH2, H3K27me3 and survivin. (A) Immunoblots of WCEs from U2OS, HeLa and MRC5 lines cultured under normoxic or hypoxic environments (24 h). Blots were immunoprobed with anti-EZH2, anti-H3K27me3 and anti-survivin antibodies. Anti-Hif1a used to prove the hypoxic state had been induced, and anti-tubulin was used as a loading control. (B–D) Quantification of immunoblots represented in A from three independent experiments demonstrating that EZH2, H3K27me3 and survivin are all more abundant under hypoxia. Data presented are means±s.d. * P <0.05, ** P <0.01, *** P <0.001 (two-way ANOVA with Tukey's multiple comparisons post test).

Article Snippet: Human cervical cancer cells (HeLa), human bone osteosarcoma cells (U2OS), retinal pigment epithelial cells (RPE) and human breast cancer cells (MCF7) were originally from ATCC.

Techniques: Expressing, Western Blot, Cell Culture, Control

Journal: Neoplasia (New York, N.Y.)

Article Title: PIK3CA mutant cervical cancer is selectively suppressed by PI3Kα inhibition (Alpelisib/BYL-719 and Inavolisib/GDC-0077) and cooperates with HPV directed T cell therapy

doi: 10.1016/j.neo.2026.101305

Figure Lengend Snippet: Impact of BYL-719 on the expression of target proteins in cervical cancer cell lines. ( A, B) CaSki cells treated with BYL-719 show reduced levels of PD-L1, YAP1, EGFR, CTGF, Integrin, and HPV16 E7. In Panel B cells were treated with 5uM BYL-719, washed at 24 h and place in 0, 1 or 5uM drug. (exposure time, 2 min). (C) BYL-719-treated ME180 cells show decreased levels of PD-L1 and CTGF. (D) SNU-17 cells also show reduced levels of these proteins after treatment (exposure time, 5 min). (E) SiHa ( PIK3CA WT) shows no reduction ofHPV16 E7 after treatment with BYL-719 (exposure time, 3 min). (F) Cell proliferation plot of SNU-17 cells treated with BYL-719. (G) SiHa cells treated with BYL719. *=P < 0.05, **=P < 0.01, ***=P < 0.001.

Article Snippet: CC cell lines, including CaSki (ATCC Cat# CRM-CRL-1550_Ca Ski, RRID: CVCL_1100), SiHa (ATCC Cat# HTB-35_SiHa, RRID: CVCL_0032), and ME180 (ATCC Cat# HTB-33_ME-180, RRID: CVCL_1401), C33A (ATCC CRM-HTB-31, RRID:CVCL_1094) were obtained from ATCC.

Techniques: Expressing

Journal: Translational Oncology

Article Title: Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells

doi: 10.1016/j.tranon.2026.102779

Figure Lengend Snippet: Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and HCC 38 cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

Article Snippet: The TNBC cell lines used in this study, including MDA-MB-231, MDA-MB-436, and HCC 38, were obtained from the American Type Culture Collection (ATCC) and maintained in our laboratory.

Techniques: CCK-8 Assay, Control, EdU Assay, Fluorescence, Flow Cytometry, Staining

Journal: Translational Oncology

Article Title: Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells

doi: 10.1016/j.tranon.2026.102779

Figure Lengend Snippet: ToxH triggers the complete autophagic process in TNBC cells. MDA-MB-231, MDA-MB-438, and HHC-38 cells were treated with or without ToxH for 24 h and transfected with or without the corresponding plasmid. (A) Western blotting detection shows an increase in the expression of LC3-II, ATG5, and Beclin-1, but a decrease in the expression of p62. (B) Immunofluorescence observation reveals that ToxH treatment generated a considerable number of LC3B puncta. (C) TNBC cells transfected with the mCherry-GFP-LC3 plasmid demonstrate an observable increase in the formation of autophagosomes (yellow puncta) and autolysosomes (red puncta) that were treated with ToxH. Data are presented as mean ± SD and analyzed using an Unpaired t-test (A) or two-way ANOVA with Tukey's multiple comparisons test (B and C), N = 3 (A) or 100 (B and C); * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

Article Snippet: The TNBC cell lines used in this study, including MDA-MB-231, MDA-MB-436, and HCC 38, were obtained from the American Type Culture Collection (ATCC) and maintained in our laboratory.

Techniques: Transfection, Plasmid Preparation, Western Blot, Expressing, Immunofluorescence, Generated

Journal: Translational Oncology

Article Title: Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells

doi: 10.1016/j.tranon.2026.102779

Figure Lengend Snippet: Combination of ToxH and CQ treatments increases anti-tumor activity through promotion of necroptosis in TNBC cells. MDA-MB-231, MDA-MB-438, and HHC-38 tumor models were established in female nude mice and treated with ToxH or combined with CQ for five mice in each group. (A) Tumor images were captured at day 18 after tumor cell inoculation. (B) Tumor volumes were measured at day 18 after the tumor cell inoculation. (C) Western blotting detection of the autophagy marker proteins LC3 and p62, and necroptosis marker proteins RIPK1, RIPK3, and MLKL and phosphorylated MLKL (pMLKL) in the tumor tissues treated with the indicated reagents. (D) Immunohistochemical detection of the necroptosis marker phosphorylated proteins pRIPK3 and pMLKL. Data are presented as mean ± SD and were assessed using one-way ANOVA with Tukey's post hoc test, where N = 5 (A and B) or representative images from triplicate experiments (C and D); * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, no significant.

Article Snippet: The TNBC cell lines used in this study, including MDA-MB-231, MDA-MB-436, and HCC 38, were obtained from the American Type Culture Collection (ATCC) and maintained in our laboratory.

Techniques: Activity Assay, Western Blot, Marker, Immunohistochemical staining

Journal: Neoplasia (New York, N.Y.)

Article Title: PIK3CA mutant cervical cancer is selectively suppressed by PI3Kα inhibition (Alpelisib/BYL-719 and Inavolisib/GDC-0077) and cooperates with HPV directed T cell therapy

doi: 10.1016/j.neo.2026.101305

Figure Lengend Snippet: Impact of BYL-719 on the expression of target proteins in cervical cancer cell lines. ( A, B) CaSki cells treated with BYL-719 show reduced levels of PD-L1, YAP1, EGFR, CTGF, Integrin, and HPV16 E7. In Panel B cells were treated with 5uM BYL-719, washed at 24 h and place in 0, 1 or 5uM drug. (exposure time, 2 min). (C) BYL-719-treated ME180 cells show decreased levels of PD-L1 and CTGF. (D) SNU-17 cells also show reduced levels of these proteins after treatment (exposure time, 5 min). (E) SiHa ( PIK3CA WT) shows no reduction ofHPV16 E7 after treatment with BYL-719 (exposure time, 3 min). (F) Cell proliferation plot of SNU-17 cells treated with BYL-719. (G) SiHa cells treated with BYL719. *=P < 0.05, **=P < 0.01, ***=P < 0.001.

Article Snippet: CC cell lines, including CaSki (ATCC Cat# CRM-CRL-1550_Ca Ski, RRID: CVCL_1100), SiHa (ATCC Cat# HTB-35_SiHa, RRID: CVCL_0032), and ME180 (ATCC Cat# HTB-33_ME-180, RRID: CVCL_1401), C33A (ATCC CRM-HTB-31, RRID:CVCL_1094) were obtained from ATCC.

Techniques: Expressing