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: 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: JACC: Basic to Translational Science

Article Title: JP2 and JCN Crosstalk Abrogate MURF1-Mediated JCN Ubiquitination and Degradation in Cardiomyocytes

doi: 10.1016/j.jacbts.2026.101534

Figure Lengend Snippet: Ca 2+ Handling in Adult Mouse Cardiomyocytes (A to C) Adult mouse cardiomyocytes were infected with Ad-JP2 or Ad-HA and exposed to palmitate or oleate. RyR2 Ca 2+ leak (F/F0), caffeine-induced peak (F/F0), and Tau-SERCA were measured. (D to F) Adult mouse cardiomyocytes were infected with Ad-JCN or Ad-HA and exposed to palmitate or oleate. RyR2 Ca 2+ leak (F/F0), Caffeine-induced peak (F/F0), and Tau-SERCA were detected. (G to I) Adult mouse cardiomyocytes were infected with Ad-shJP2 or Ad-HA. RyR2 Ca 2+ leak (F/F0), caffeine-induced peak (F/F0), and Tau-SERCA were detected. (J to L) Adult mouse cardiomyocytes were infected with Ad-AsJCN or Ad-HA. RyR2 Ca 2+ leak (F/F0), caffeine-induced peak (F/F0), and Tau-SERCA were determined. Data are mean ± SD, n = 9-11 different adult mouse cardiomyocytes in each group. Two-way analysis of variance followed by Newman-Keuls post hoc test was performed for multiple pairwise comparisons. Student's t -test was used for comparison between 2 groups. ∗ P < 0.05 vs Ad-HA or oleate + Ad-HA, and † P < 0.05 vs palmitate + Ad-HA. ∗ and †: P < 0.05; ∗∗ and ††: P < 0.01; ∗∗∗ and †††: P < 0.001. Abbreviations as in .

Article Snippet: Then, sarcoplasmic reticulum (SR) Ca 2+ leak via RyRs was estimated in 0 Ca 2+ /0 Na + Tyrode's solution containing tetracaine (1 mmol/L, MedChemExpress, HY-A0079).

Techniques: Infection, Comparison

Journal: JACC: Basic to Translational Science

Article Title: JP2 and JCN Crosstalk Abrogate MURF1-Mediated JCN Ubiquitination and Degradation in Cardiomyocytes

doi: 10.1016/j.jacbts.2026.101534

Figure Lengend Snippet: Schematic Mechanism In normal conditions, JP2 binds to JCN and blocks the MURF1-JCN interaction, thereby preventing MURF1-mediated ubiquitination and proteasome-dependent degradation of JCN. However, the protein level of JP2 is reduced under stress, enabling MURF1 to bind to JCN and promoting MURF1-mediated ubiquitination and degradation of JCN. JCN reduction triggers the excessive opening and Ca 2+ release from RyR2, leading to cardiomyocyte injury. In contrast, overexpression of JP2 or JCN protects intracellular Ca 2+ homeostasis and prevents cell death under stress.

Article Snippet: Then, sarcoplasmic reticulum (SR) Ca 2+ leak via RyRs was estimated in 0 Ca 2+ /0 Na + Tyrode's solution containing tetracaine (1 mmol/L, MedChemExpress, HY-A0079).

Techniques: Ubiquitin Proteomics, Over Expression