Journal: International Journal of Molecular Sciences

Article Title: Enhanced Anti-Tumor Activity of Cetuximab-Modified Nanostructured Lipid Carriers Loaded with Para -Quinone Methide Derivative p -QM-1h

doi: 10.3390/ijms27083674

Figure Lengend Snippet: The effects of CTX- p -QM-1h-NLC on the expressions of TrxR, Bax and Caspase-3 in tumors of 4T1 tumor-bearing Balb/c mice. ( A ) Representative target protein bands. The experiment was performed at least in triplicate. ( B ) Relative ratio of TrxR. ( C ) Relative ratio of Bax. ( D ) Relative ratio of Caspase-3. The grayscale quantitative analyses of the expressions of TrxR, Bax and Caspase-3 were performed using the ImageJ software (1.53e). Error bars represent mean ± SD. * p < 0.05, ** p < 0.01 and *** p < 0.001 compared with the model group.

Article Snippet: The primary antibodies used in the experiments were as follows: TrxR (bs-8299R, Bioss, Beijing, China), Bax (bsm-52316R, Bioss, Beijing, China), Caspase-3 (bsm-61071R, Bioss, Beijing, China) and β-actin (GB15003, Servicebio, Wuhan, China).

Techniques: Software

Journal: bioRxiv

Article Title: Cell state-specific metabolic networks govern ferroptosis versus apoptosis in small cell lung cancer

doi: 10.64898/2026.03.27.714827

Figure Lengend Snippet: A. Representative immunoassay (n=3) for the marker of apoptosis cleaved caspase 3 (CC3) for ASCL1 high mSCLC cells in response to low Cys levels in the medium, as indicated. HSP90 was used as a loading control. B. Average viability (AlamarBlue assay) of RPR2 -derived ASCL1 high mSCLC cells cultured in Cys-depleted medium supplemented with Boc-D-FMK [50 µM], Fer-1 [1 µM], chloroquine (CQ) [20 µM], and GSH-MEE [100 µM], as percent of the cells in complete medium (n=3). C. Cell death (DRAQ7 count/confluence in %) of RP -derived ASCL1 high mSCLC cells (181.5 FL, 246.7 FL). Cells were cultured in Cys-depleted medium supplemented with Cys [200 µM], Emricasan (Emri.) [2.5 µM], QVD [10 µM] and Fer-1 [1 µM] for 24 h. D. Representative immunoassay (n=3) for CC3 in ASCL1 high (NCI-DMS79, NCI-H187, NCI-H146) and NEUROD1 high (NCI-H82, NCI-H524) hSCLC cell lines in Cys replete [100 µM] or Cys-depleted medium. HSP90 was used as a loading control. E,F. Cell death (DRAQ7 count/confluence in %) of ASCL1 high and ASCL1 low hSCLC cell lines as indicated. Cells were cultured in Cys-depleted medium, supplemented with Cys [200 µM], Emricasan [2.5 µM], and QVD [10 µM] for 72 h. G. Scheme summarizing the consequences of Cys depletion in the different SCLC subtypes. For (B), P-value was calculated by the unpaired Student’s t-test. For (C,E,F) one-way ANOVA was performed, and Tukey was used as post hoc test. Error bars indicate mean ± SEM.

Article Snippet: Sections were then incubated overnight at 4°C with anti-cleaved caspase-3 rabbit monoclonal antibody (Cell Signaling Technology, #9661, 1:500 dilution) diluted in blocking buffer supplemented with biotin and PBS.

Techniques: Marker, Control, Alamar Blue Assay, Derivative Assay, Cell Culture

Journal: bioRxiv

Article Title: Cell state-specific metabolic networks govern ferroptosis versus apoptosis in small cell lung cancer

doi: 10.64898/2026.03.27.714827

Figure Lengend Snippet: A. Final volume measurements of the individual tumors in . B. Final volume measurements of the individual tumors in . C. Final volume measurements of the individual tumors in . D. Representative images of sections from RU1322 and RU443 tumors immunostained with cleaved caspase 3 (CC3) and 4-HNE antibodies. Scale bars, 100 µm. E. Quantifications of 4-HNE in sections from RU433 tumors (n(control)=11, n(No Cys)=6, n(DAHP)=6, n(combo)=5). F. Quantifications of 4-HNE in sections from RU1322 tumors (n(control)=7, n(No Cys)=4, n(DAHP)=4, n(combo)=5). G. Quantifications of CC3 in sections from RU433 tumors (n(control)=11, n(No Cys)=5, n(DAHP)=6, n(combo)=5). H. Quantifications of CC3 in sections from RU1322 tumors (n(control)=7, n(No Cys)=4, n(DAHP)=4, n(combo)=5). For (A, B, C) one-way ANOVA was performed followed by the unpaired Student’s t-test for post hoc analysis. For (E,F,G,H) one-way ANOVA was performed, and Tukey was used as post hoc test. Error bars indicate mean ± SEM.

Article Snippet: Sections were then incubated overnight at 4°C with anti-cleaved caspase-3 rabbit monoclonal antibody (Cell Signaling Technology, #9661, 1:500 dilution) diluted in blocking buffer supplemented with biotin and PBS.

Techniques: Control

Journal: bioRxiv

Article Title: Cell state-specific metabolic networks govern ferroptosis versus apoptosis in small cell lung cancer

doi: 10.64898/2026.03.27.714827

Figure Lengend Snippet: A. Growth of patient-derived xenograft (PDX), LX674C (ASCL1 high ), treated with vehicle, No Cys (cysteinase 50 mg/kg, q.2.d., i.p., and Cys-depleted diet), DAHP (25 mg/kg, q.2.d., i.p.), or both, for 14 days (n=6 mice with two tumors each). B. Same as above with PDX, RU443 (NEUROD1 high ). C. Same as above with PDX, RU1322 (POU2F3 high ). D. Representative images of sections from LX674C tumors immunostained with cleaved caspase 3 (CC3) and 4-HNE antibodies. Scale bars, 100 µm. E. Quantifications of 4-HNE and CC3 tumor sections as in (d) (n(control)=7, n(No Cys)=4, n(DAHP)=6, n(combo)=10). F. High expression of GCH1 correlates with sensitivity to ABT-199 (venetoclax), and inversely with the ferroptosis inducers ML210, Erastin and RSL3 in human SCLC cell lines. Plotted values are z-scored Pearson’s correlation coefficients; line, median; box, 25th to 75th percentile; whiskers, 2.5th and 97.5th percentile expansion. Data from the CTRP database. G. Growth of DMS79 human SCLC xenografts treated with No Cys (cysteinase 50 mg/kg, q.2.d., i.p., and Cys-depleted diet), venetoclax (25 mg/kg, q.i.w., p.o.), or both, for 14 days (n=20). H. Model. SCLC tumors are dependent on importing extracellular Cys because they lack expression of the GNMT enzyme in the transmethylation pathway. Under conditions where Cys is available for import, SCLC cells in all states (ASCL1 high and NEUROD1 high neuroendocrine cells, as well as non-neuroendocrine cells) proliferate and survive. In the absence of exogenous Cys, ASCL1 high cells are protected from ferroptosis because ASCL1 directly upregulates the transcription of the gene coding for GCH1, an enzyme critical to produce the antioxidant metabolite BH4. ASCL1 high SCLC cells can die from ferroptosis when GCH1 is inhibited or can be pushed towards more apoptotic cell death in the absence of Cys using molecules such as BCL-2 inhibitors. ASCL1 low SCLC cells die from ferroptosis upon Cys depletion, and this death can be further enhanced by oxidative stress, including chemotherapy. For (E) one-way analysis of variance (ANOVA) was performed (P<0.0001), and Tukey was used as post hoc test. For all other figures, two-way ANOVA was performed (P<0.0001), followed by the unpaired Student’s t-test. Error bars indicate mean ± SEM.

Article Snippet: Sections were then incubated overnight at 4°C with anti-cleaved caspase-3 rabbit monoclonal antibody (Cell Signaling Technology, #9661, 1:500 dilution) diluted in blocking buffer supplemented with biotin and PBS.

Techniques: Derivative Assay, Control, Expressing