Fig 2: Resensitization to chemotherapeutic killing by 102-5 anti-CLPTM1L.a Western blotting of cisplatin-sensitive and resistant ovarian tumor cell lysates for CLPTM1L and analysis of dose–response of phospho-Akt and total Akt to 102-5 anti-CLPTM1L treatment. b Dose–response analyses and cisplatin IC50s of cisplatin-sensitive and resistant human ovarian tumor cells. Error bars represent standard error of the mean. Akt phosphorylation levels in resistant versus resistant lines are shown in insets. c Flow cytometry on A2780 detecting cell surface CLPTM1L with 102-5 human anti-CLPTM1L. d Kinetic killing assay (live imaging) in A2780 with human anti-CLPTM1L and/or 10 µM carboplatin treatment. Error bars represent standard error of the mean. *p < 0.05, **p < 0.005, ***p < 0.0005. e Western blotting for Akt and phospho-Akt (T308) in A2780 and HeyA8 resistant cell lines treated with 102-5 anti-CLPTM1L and/or cisplatin. f Cisplatin dose–response curves for MCW-OV-SL3 sensitive (parental) and resistant (MCW-OV-SL3-CisR) tumor spheroids, pAkt (T308) and total Akt western blots on MCW-OV-SL3 and MCW-OV-SL3-CisR spheroid lysates (inset). Error bars represent standard error of the mean. g Viability (MTT) of MCW-OV-SL3-CisR spheroids after 16 days of growth, treated with cisplatin and/or 102-5 anti-CLPTM1L at the indicated concentrations beginning at 4 days post-seeding. *p < 0.05, **p < 0.005. h Photomicrographs of MCW-OV-SL3-CisR spheroids after 16 days of growth, treated with cisplatin and/or 102-5 anti-CLPTM1L. i Western blotting of MCW-OV-SL3-CisR spheroid lysates for caspase cleavage and Akt phosphorylation after 16 days of growth, treated with cisplatin and/or 102-5 anti-CLPTM1L. j Western blotting of MCW-OV-SL3-CisR monolayer cultures for phospho- and total Akt following treatment with control (PSB) or 102-5 anti-CLPTM1L at the indicated concentrations.

Fig 3: Kaplan–Meier graphs representing the probability of OSCC patients’ survival based on CLPTM1L expression status. (A) High CLPTM1L expression is significantly associated with reduced overall survival in OSCC patients. (B) High CLPTM1L expression is significantly associated with reduced disease-free survival in OSCC patients. P-value from Log-rank test is shown.

Fig 4: CLPTM1L expression and outcome.a CLPTM1L IHC on a representative human ovarian serous adenocarcinoma. Negative CT: secondary antibody staining only. Bars = 50 µM. b IHC staining indices for ovarian serous adenocarcinoma (n = 24) (represented in ‘a’) and FNA normal human tissues n = 144 (n = 4 per tissue). Bars represent means, and error bars represent standard error of the mean. c CLPTM1L staining on each of 11 patient-derived xenograft tissues. Negative control in the lower right panel was performed on the same patient and section as in the lower left panel. Scale bars = 50 µM. d Copy number variation (CNV) of CLPTM1L in various cancer cell lines analyzed using the depmap portal (https://depmap.org/portal). Box limits represent upper and lower quartiles. Whiskers represent 1.5× inter-quartile range. Points represent outliers. e Western blotting for CLPTM1L in human ovarian cancer PDX, endothelial, normal fallopian tube epithelial cells, pancreatic fibroblasts, and different tumor cell lines. f Progression free survival. g Overall survival. h Overall survival in patients with CA125 < lower quartile as analyzed using KM Plot.

Fig 5: Immunohistochemistry was used to detect the typical expression of CLPTM1L. (A, B) Normal oral epithelium tissue showed negative expression of CLPTM1L. (C, D) primary oral squamous cell carcinoma showed low and high expression of CLPTM1L. (E, F) primary oral squamous cell carcinoma showed low and high expression of CLPTM1L. (Scale: 100 µm).