Journal: Frontiers in Pharmacology

Article Title: A pan-cancer analysis of the expression and molecular mechanism of DHX9 in human cancers

doi: 10.3389/fphar.2023.1153067

Figure Lengend Snippet: Differential expression patteerns of DHX9 across various cancers and pathological stages. (A) Based on the TCGA dataset, the DHX9 expression in different cancers through TIMER2. (B) For the type of DLBC, LGG, and THYM in the TCGA project, we used the GTEx database to provide the corresponding normal tissues as controls. The box plot data of comparison between tumor and normal tissues were supplied. (C) The DHX9 expression in different pathological stages of ACC, LIHC and SKCM. (D) The protein expression levels of DHX9 between tumor and normal tissues of breast cancer, ovarian cancer, colon cancer, ccRCC, UCEC, and LUAD. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: Liver cancer cells Hep-3B and SK-Hep-1 were purchased from the Chinese Academy of Science Cell Bank (Shanghai, China). ccRCC cells ACHN and OS-RC-2 were purchased form Icellbioscience (Shanghai, China).

Techniques: Quantitative Proteomics, Expressing, Comparison

Journal: Frontiers in Pharmacology

Article Title: A pan-cancer analysis of the expression and molecular mechanism of DHX9 in human cancers

doi: 10.3389/fphar.2023.1153067

Figure Lengend Snippet: DHX9 mediates the proliferation, metastasis and EMT process of cancer cells. (A) Representative images and quantitative analysis of the colony formation assay for transfected Hep-3B/H1299/MDA-MB-231/ACHN cells. (B) Representative images and quantitative analysis of the transwell assay for transfected Hep-3B/H1299/MDA-MB-231/ACHN cells. (C–E) Representative images and quantitative analysis of the Wound healing assay for transfected Hep-3B/H1299/MDA-MB-231/ACHN cells. (F) Western blot visualization of altered expression of EMT related molecules after knockdown DHX9 in Hep-3B, H1299, MDA-MB-231and ACHN cell lines. (G) The efficiency of silencing DHX9 was indicated by RT-qPCR in Hep-3B, H1299, MDA-MB-231, and ACHN cell lines. (H, I) Representative images and quantitative analysis of tumors in vivo experiments. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: Liver cancer cells Hep-3B and SK-Hep-1 were purchased from the Chinese Academy of Science Cell Bank (Shanghai, China). ccRCC cells ACHN and OS-RC-2 were purchased form Icellbioscience (Shanghai, China).

Techniques: Colony Assay, Transfection, Transwell Assay, Wound Healing Assay, Western Blot, Expressing, Knockdown, Quantitative RT-PCR, In Vivo

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: The depletion of CCT3 impairs the abilities of proliferation, migration, and invasion in ccRCC cells (A) Western blot analysis was performed to assess the protein expression of CCT3 in four pairs of clear cell renal cell carcinoma tissues (T) and their corresponding adjacent normal tissues (N). ( n = 4). (B) The immunohistochemical results of CCT3 in ccRCC and normal renal tissue in the HPA database. (C) Western blot was used to assess the effects of two distinct CCT3 knockdown sequences in 786-O and 769-P cells. (D and E) Wound-healing assay indicates that CCT3 knockdown suppresses the viability of 786-O and 769-P cells. (F and G) Transwell assay indicates impaired abilities of migration and invasion of 769-P and 786-O cells. (H and I) The proliferative abilities of stably CCT3-depleted 769-P and 786-O cells were measured with an EdU staining assay. (Scale bars, 100 μm. Data in C-I are presented as the means ± SDs ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). Two-tailed Student’s t test for A, Student’s t test for C-I.

Article Snippet: The cell lines 786-O, 769-P, A498 and OSRC2 were provided by Procell (Procell LifeScience & Technology Co., Ltd).

Techniques: Migration, Western Blot, Expressing, Immunohistochemical staining, Knockdown, Wound Healing Assay, Transwell Assay, Stable Transfection, Staining, Two Tailed Test

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: Knockdown of XPO1 inhibited the invasion and migration abilities of ccRCC cells (A) The Venn diagram obtained by taking the intersection of the relevant gene sets of CCT3 and RB1 after screening. (B) Expression level of XPO1 in clear cell RCC from the TCGA database. (C) The immunohistochemical results of XPO1 in ccRCC and normal renal tissue in the HPA database. (D) A Kaplan-Meier curve illustrates OS in patients with ccRCC from low and high XPO1 expression groups. (E) The promoter methylation level of XPO1 in KIRC from the TCGA database. (F) Western blot analysis was performed to assess the protein expression of XPO1 in CCT3-depleted cells. (G) Using Spearman correlation analysis, the correlation between Gene CCT3 and XPO1 expression, and the correlation between XPO1 and RB1 expression. (H) Wound-healing assay indicates that XPO1 knockdown suppresses the viability of 786-O and 769-P cells. (I) Transwell assay indicates impaired abilities of migration and invasion of 769-P and 786-O cells. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). Two-tailed Student’s t test for B and E. Student’s t test for F, H, and I.

Article Snippet: The cell lines 786-O, 769-P, A498 and OSRC2 were provided by Procell (Procell LifeScience & Technology Co., Ltd).

Techniques: Knockdown, Migration, Expressing, Immunohistochemical staining, Methylation, Western Blot, Wound Healing Assay, Transwell Assay, Two Tailed Test

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: The reduction of XPO1 induces cellular senescence in ccRCC cells (A) Western blot analysis was performed to assess the protein expression of CDK4, CyclinD, p-Rb (Ser807/811) in XPO1 knockdown cells. (B) The mRNA expression levels of senescence-associated genes, including interleukin 1 A, TNF, CDK2, CDK4, and CDK6 in XPO1-depleted cells were examined by qRT-PCR. (C) Changes of SA-β-gal activity in XPO1-knockdown cells. Data represent the percentage of cells staining positive for SA-β-gal ±SD. (D) Cell cycle analysis calculated the distribution of the cells in G1, S, and G2/M phases. (E) The proliferative abilities of 769-P and 786-O cells, which were treated with the XPO1 inhibitor Selinexor, were measured with an EdU staining assay. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). Student’s t test.

Article Snippet: The cell lines 786-O, 769-P, A498 and OSRC2 were provided by Procell (Procell LifeScience & Technology Co., Ltd).

Techniques: Western Blot, Expressing, Knockdown, Quantitative RT-PCR, Activity Assay, Staining, Cell Cycle Assay