Journal: Translational Lung Cancer Research

Article Title: CDKN1A promotes paclitaxel resistance through mediating formation of polyploid giant cancer cells and enhancing neosis in non-small cell lung cancer

doi: 10.21037/tlcr-2026-1-0155

Figure Lengend Snippet: PTX induces the formation of PGCCs in NSCLC. (A) The process of PTX induced PGCCs in lung cancer cells and the experimental design and morphological changes of daughter cells by phase contrast microscope. PGCCs (black arrows) appeared on day 4 after PTX treatment, budded on day 8 (green arrows), and formed a large number of daughter cells on day 10 (red arrows). (B) Flow cytometry assays were used to detect the changes in PGCCs content at different time points during PTX treatment. (C) The ratios of PGCCs were shown. (D) The process of PTX induced PGCCs in lung cancer cells and the production of daughter cells were observed under laser confocal microscopy. Scale bar, 10 μm. (E) Quantitative analyses of cell surface area for A549 vs. A549-P vs. A549-D. Data were presented as mean ± SD; statistical significance was assessed using a Student’s t -test. ***, P<0.001; ****, P<0.0001. A549-P, A549-PGCCs; A549-D, A549-daughter cells. DAPI, 4',6-diamidino-2-phenylindole; NSCLC, non-small cell lung cancer; PTX, paclitaxel; PGCC, polyploid giant cancer cell; SD, standard deviation.

Article Snippet: When A549 and H1299 cells reached 80% confluency, PTX (Bristol Myers Squibb, Princeton, NJ, USA) was added at a final concentration of 60 ng/mL, and continued to culture for another 18 h. After removing the PTX-containing medium, phosphate-buffered saline (PBS) (Cat No. C0221A, Beyotime, Shanghai, China) was added to wash the cells and then replaced them with regular culture medium.

Techniques: Microscopy, Flow Cytometry, Confocal Microscopy, Standard Deviation

Journal: Translational Lung Cancer Research

Article Title: CDKN1A promotes paclitaxel resistance through mediating formation of polyploid giant cancer cells and enhancing neosis in non-small cell lung cancer

doi: 10.21037/tlcr-2026-1-0155

Figure Lengend Snippet: CDKN1A mediates the formation of PGCCs induced by paclitaxel. (A,B) Interference efficiency of CDKN1A was detected by qPCR and Western blot in A549 (A) and H1299 (B). (C) The ratios of PGCCs were statistically shown. Each bar represents the mean ± SD of three independent experiments. Student’s t -test was used to determine statistical significance. (D) Western blot was used to detect the expression changes of CDKN1A under different concentrations of UC2288 inhibitor treatment. (E) Quantification of PGCCs number after UC2288 treatment. (F) The morphological changes induced by PTX in lung cancer cell PGCCs and daughter cells at different time points after treatment with UC2288 were observed by phase contrast microscope. (G) The morphological changes induced by PTX in PGCCs and daughter cells of lung cancer cells were observed under laser confocal microscopy after treatment with UC2288 at different time points. Scale bar, 10 μm. (H) Quantification analysis of tumor cell surface area following PTX and UC2288 treatment over time. **, P<0.01; ***, P<0.001. DAPI, 4',6-diamidino-2-phenylindole; PGCC, polyploid giant cancer cell; PTX, paclitaxel; qPCR, quantitative polymerase chain reaction; SD, standard deviation.

Article Snippet: When A549 and H1299 cells reached 80% confluency, PTX (Bristol Myers Squibb, Princeton, NJ, USA) was added at a final concentration of 60 ng/mL, and continued to culture for another 18 h. After removing the PTX-containing medium, phosphate-buffered saline (PBS) (Cat No. C0221A, Beyotime, Shanghai, China) was added to wash the cells and then replaced them with regular culture medium.

Techniques: Western Blot, Expressing, Microscopy, Confocal Microscopy, Real-time Polymerase Chain Reaction, Standard Deviation