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human ccrcc cell lines (ATCC)

Name: human ccrcc cell lines
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ATCC human ccrcc cell lines

The highly expressed sialylation-immune-related lncRNA LINC01605 in <t>ccRCC</t> correlates with poor prognosis. (A) 66 overlapping lncRNAs associated with SRGs, immune cells, phenotypes, and prognosis were identified in a Venn diagram for further investigation. (B) C-index of prognostic models constructed by multiple machine learning methods. (C) Forest plot displaying univariate Cox regression analysis results for 12 SIRLs in OS, PFI, and DSS. The HR values along with their corresponding 95% confidence intervals are shown. (D) Kaplan-Meier plots for overall survival (OS), progression-free interval (PFI), and disease-specific survival (DSS) were generated using the median expression of LINC01605 as the cut-off. (E) Relative RNA expression of LINC01605 in 10 pairs of <t>human</t> <t>ccRCC</t> tumors (n = 10 per group). (F) FISH-IF detected LINC01605 expression in tumor and adjacent non-tumor tissues of ccRCC patients, with CA9 as the ccRCC cell marker. (G) Expression levels of LINC01605 in HK-2 and different ccRCC cell lines were detected (n = 3 per group). (H) GSEA revealed high LINC01605 expression to be functionally associated with enriched cell proliferation, stemness, migration, and invasion pathways. All bioinformatics analyses in <xref ref-type=

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Article Title: Sialylation-immune-related lncRNA LINC01605 promotes tumor-infiltrating CD8 + T cell exhaustion and malignancy of clear cell renal cell carcinoma

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2025.1744278

The highly expressed sialylation-immune-related lncRNA LINC01605 in ccRCC correlates with poor prognosis. (A) 66 overlapping lncRNAs associated with SRGs, immune cells, phenotypes, and prognosis were identified in a Venn diagram for further investigation. (B) C-index of prognostic models constructed by multiple machine learning methods. (C) Forest plot displaying univariate Cox regression analysis results for 12 SIRLs in OS, PFI, and DSS. The HR values along with their corresponding 95% confidence intervals are shown. (D) Kaplan-Meier plots for overall survival (OS), progression-free interval (PFI), and disease-specific survival (DSS) were generated using the median expression of LINC01605 as the cut-off. (E) Relative RNA expression of LINC01605 in 10 pairs of human ccRCC tumors (n = 10 per group). (F) FISH-IF detected LINC01605 expression in tumor and adjacent non-tumor tissues of ccRCC patients, with CA9 as the ccRCC cell marker. (G) Expression levels of LINC01605 in HK-2 and different ccRCC cell lines were detected (n = 3 per group). (H) GSEA revealed high LINC01605 expression to be functionally associated with enriched cell proliferation, stemness, migration, and invasion pathways. All bioinformatics analyses in <xref ref-type=

Figure 1 were based on the gene expression data (TPM values) and clinical data of 528 ccRCC samples from the TCGA-KIRC cohort. Values are presented as mean ± SD. P -values were calculated by log-rank (Mantel-Cox) test (D) , two-tailed paired Student’s t-test (E) , one-way ANOVA followed Tukey’s multiple comparisons (G) , or non-parametric permutation test (H) . *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant. n represents the number of biological replicates in (E, G) . " title="The highly expressed sialylation-immune-related lncRNA LINC01605 in ccRCC correlates with poor prognosis. (A) 66 overlapping lncRNAs ..." property="contentUrl" width="100%" height="100%"/>
Figure Legend Snippet: The highly expressed sialylation-immune-related lncRNA LINC01605 in ccRCC correlates with poor prognosis. (A) 66 overlapping lncRNAs associated with SRGs, immune cells, phenotypes, and prognosis were identified in a Venn diagram for further investigation. (B) C-index of prognostic models constructed by multiple machine learning methods. (C) Forest plot displaying univariate Cox regression analysis results for 12 SIRLs in OS, PFI, and DSS. The HR values along with their corresponding 95% confidence intervals are shown. (D) Kaplan-Meier plots for overall survival (OS), progression-free interval (PFI), and disease-specific survival (DSS) were generated using the median expression of LINC01605 as the cut-off. (E) Relative RNA expression of LINC01605 in 10 pairs of human ccRCC tumors (n = 10 per group). (F) FISH-IF detected LINC01605 expression in tumor and adjacent non-tumor tissues of ccRCC patients, with CA9 as the ccRCC cell marker. (G) Expression levels of LINC01605 in HK-2 and different ccRCC cell lines were detected (n = 3 per group). (H) GSEA revealed high LINC01605 expression to be functionally associated with enriched cell proliferation, stemness, migration, and invasion pathways. All bioinformatics analyses in Figure 1 were based on the gene expression data (TPM values) and clinical data of 528 ccRCC samples from the TCGA-KIRC cohort. Values are presented as mean ± SD. P -values were calculated by log-rank (Mantel-Cox) test (D) , two-tailed paired Student’s t-test (E) , one-way ANOVA followed Tukey’s multiple comparisons (G) , or non-parametric permutation test (H) . *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant. n represents the number of biological replicates in (E, G) .

Techniques Used: Construct, Generated, Expressing, RNA Expression, Marker, Migration, Gene Expression, Two Tailed Test

LINC01605 is associated with the malignant progression of ccRCC cells. (A) LINC01605 was silenced in A498 and 786-O cell lines by two different shRNAs (n = 3 per group). (B, C) CCK8 and colony formation assays were performed in LINC01605 -knockdown and counterpart control groups (n = 3 per group). (D, E) Transwell migration/invasion and wound-healing assays showed that knockdown of LINC01605 impaired mobility and invasiveness of ccRCC cell lines (n = 3 per group). (F) EdU assay showed that cell proliferation and DNA synthesis decreased in LINC01605 -silenced ccRCC cell lines (n = 3 per group). (G) Knockdown of LINC01605 in A498 cells inhibited the growth of A498-derived xenograft in vivo (n = 5 per group). Tumor growth curves, tumor weights and statistical analysis are shown. Values are presented as mean ± SD. P -values were determined by one-way ANOVA followed Tukey’s multiple comparisons [ (A-G) one comparison per time point for (B , G) ]. *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant. n represents the number of biological replicates in (A-G) .

Figure Legend Snippet: LINC01605 is associated with the malignant progression of ccRCC cells. (A) LINC01605 was silenced in A498 and 786-O cell lines by two different shRNAs (n = 3 per group). (B, C) CCK8 and colony formation assays were performed in LINC01605 -knockdown and counterpart control groups (n = 3 per group). (D, E) Transwell migration/invasion and wound-healing assays showed that knockdown of LINC01605 impaired mobility and invasiveness of ccRCC cell lines (n = 3 per group). (F) EdU assay showed that cell proliferation and DNA synthesis decreased in LINC01605 -silenced ccRCC cell lines (n = 3 per group). (G) Knockdown of LINC01605 in A498 cells inhibited the growth of A498-derived xenograft in vivo (n = 5 per group). Tumor growth curves, tumor weights and statistical analysis are shown. Values are presented as mean ± SD. P -values were determined by one-way ANOVA followed Tukey’s multiple comparisons [ (A-G) one comparison per time point for (B , G) ]. *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant. n represents the number of biological replicates in (A-G) .

Techniques Used: Knockdown, Control, Migration, EdU Assay, DNA Synthesis, Derivative Assay, In Vivo, Comparison

LINC01605 is associated with sialic acid levels and involved in JAK3/STAT3 signaling. (A, B) Uniform manifold approximation and projection (UMAP) plots of ccRCC samples and tumor-infiltrating CD8 + T cell subpopulation. (C) ccRCC samples with highly sialylated tumor cells had higher exhaustion scores and lower effector and cytotoxicity scores in the corresponding CD8 + T cell subpopulation. (D) Flow cytometry results indicated that LINC01605 silencing decreased sialic acid levels on the cell membrane of A498 and 786-O cell lines (n = 5 per group). (E) qRT-PCR and western blotting showed that LINC01605 expression was correlated with mRNA and protein expression of ST6GALNAC5 (n = 3 per group). (F) GSEA analysis in the TCGA-KIRC cohort (n=528) revealed that high LINC01605 expression was related to the IL6/JAK/STAT3 and MYC target pathways. (G) The mRNA expression of JAK3 and STAT3 was detected using qRT-PCR in LINC01605 -silenced ccRCC cell lines (n = 3 per group). (H) Western blotting was performed to detect the expression of JAK3, STAT3, phosphorylated STAT3, and downstream genes of the pathway after LINC01605 knockdown in ccRCC cell lines. (I) Binding sites of STAT3 at the ST6GALNAC5 promoter were predicted by JASPAR. (J) ChIP assays demonstrated that STAT3 bound to the ST6GALNAC5 promoter in A498 and 786-O cells (n = 3 per group). Values are presented as mean ± SD. P -values were calculated by two-tailed unpaired Student’s t-test (C, J) , one-way ANOVA followed Tukey’s multiple comparisons (D, E, G) , or non-parametric permutation test (F) . *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant. n represents the number of samples in (F) and the number of biological replicates in (D-E, G, J) .

Figure Legend Snippet: LINC01605 is associated with sialic acid levels and involved in JAK3/STAT3 signaling. (A, B) Uniform manifold approximation and projection (UMAP) plots of ccRCC samples and tumor-infiltrating CD8 + T cell subpopulation. (C) ccRCC samples with highly sialylated tumor cells had higher exhaustion scores and lower effector and cytotoxicity scores in the corresponding CD8 + T cell subpopulation. (D) Flow cytometry results indicated that LINC01605 silencing decreased sialic acid levels on the cell membrane of A498 and 786-O cell lines (n = 5 per group). (E) qRT-PCR and western blotting showed that LINC01605 expression was correlated with mRNA and protein expression of ST6GALNAC5 (n = 3 per group). (F) GSEA analysis in the TCGA-KIRC cohort (n=528) revealed that high LINC01605 expression was related to the IL6/JAK/STAT3 and MYC target pathways. (G) The mRNA expression of JAK3 and STAT3 was detected using qRT-PCR in LINC01605 -silenced ccRCC cell lines (n = 3 per group). (H) Western blotting was performed to detect the expression of JAK3, STAT3, phosphorylated STAT3, and downstream genes of the pathway after LINC01605 knockdown in ccRCC cell lines. (I) Binding sites of STAT3 at the ST6GALNAC5 promoter were predicted by JASPAR. (J) ChIP assays demonstrated that STAT3 bound to the ST6GALNAC5 promoter in A498 and 786-O cells (n = 3 per group). Values are presented as mean ± SD. P -values were calculated by two-tailed unpaired Student’s t-test (C, J) , one-way ANOVA followed Tukey’s multiple comparisons (D, E, G) , or non-parametric permutation test (F) . *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant. n represents the number of samples in (F) and the number of biological replicates in (D-E, G, J) .

Techniques Used: Flow Cytometry, Membrane, Quantitative RT-PCR, Western Blot, Expressing, Knockdown, Binding Assay, Two Tailed Test

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Journal: Frontiers in Immunology

Article Title: Sialylation-immune-related lncRNA LINC01605 promotes tumor-infiltrating CD8 + T cell exhaustion and malignancy of clear cell renal cell carcinoma

doi: 10.3389/fimmu.2025.1744278

Figure Lengend Snippet: The highly expressed sialylation-immune-related lncRNA LINC01605 in ccRCC correlates with poor prognosis. (A) 66 overlapping lncRNAs associated with SRGs, immune cells, phenotypes, and prognosis were identified in a Venn diagram for further investigation. (B) C-index of prognostic models constructed by multiple machine learning methods. (C) Forest plot displaying univariate Cox regression analysis results for 12 SIRLs in OS, PFI, and DSS. The HR values along with their corresponding 95% confidence intervals are shown. (D) Kaplan-Meier plots for overall survival (OS), progression-free interval (PFI), and disease-specific survival (DSS) were generated using the median expression of LINC01605 as the cut-off. (E) Relative RNA expression of LINC01605 in 10 pairs of human ccRCC tumors (n = 10 per group). (F) FISH-IF detected LINC01605 expression in tumor and adjacent non-tumor tissues of ccRCC patients, with CA9 as the ccRCC cell marker. (G) Expression levels of LINC01605 in HK-2 and different ccRCC cell lines were detected (n = 3 per group). (H) GSEA revealed high LINC01605 expression to be functionally associated with enriched cell proliferation, stemness, migration, and invasion pathways. All bioinformatics analyses in Figure 1 were based on the gene expression data (TPM values) and clinical data of 528 ccRCC samples from the TCGA-KIRC cohort. Values are presented as mean ± SD. P -values were calculated by log-rank (Mantel-Cox) test (D) , two-tailed paired Student’s t-test (E) , one-way ANOVA followed Tukey’s multiple comparisons (G) , or non-parametric permutation test (H) . *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant. n represents the number of biological replicates in (E, G) .

Article Snippet: The human embryonic kidney 293T cell line (293T), immortalized renal epithelial cell line (HK-2), and the human ccRCC cell lines (Caki-1, 769-P, Caki-2, 786-O, A-498 and RCCJF) were obtained from the American Type Culture Collection (ATCC).

Techniques: Construct, Generated, Expressing, RNA Expression, Marker, Migration, Gene Expression, Two Tailed Test

Journal: Frontiers in Immunology

Article Title: Sialylation-immune-related lncRNA LINC01605 promotes tumor-infiltrating CD8 + T cell exhaustion and malignancy of clear cell renal cell carcinoma

doi: 10.3389/fimmu.2025.1744278

Figure Lengend Snippet: LINC01605 is associated with the malignant progression of ccRCC cells. (A) LINC01605 was silenced in A498 and 786-O cell lines by two different shRNAs (n = 3 per group). (B, C) CCK8 and colony formation assays were performed in LINC01605 -knockdown and counterpart control groups (n = 3 per group). (D, E) Transwell migration/invasion and wound-healing assays showed that knockdown of LINC01605 impaired mobility and invasiveness of ccRCC cell lines (n = 3 per group). (F) EdU assay showed that cell proliferation and DNA synthesis decreased in LINC01605 -silenced ccRCC cell lines (n = 3 per group). (G) Knockdown of LINC01605 in A498 cells inhibited the growth of A498-derived xenograft in vivo (n = 5 per group). Tumor growth curves, tumor weights and statistical analysis are shown. Values are presented as mean ± SD. P -values were determined by one-way ANOVA followed Tukey’s multiple comparisons [ (A-G) one comparison per time point for (B , G) ]. *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant. n represents the number of biological replicates in (A-G) .

Techniques: Knockdown, Control, Migration, EdU Assay, DNA Synthesis, Derivative Assay, In Vivo, Comparison

Journal: Frontiers in Immunology

Article Title: Sialylation-immune-related lncRNA LINC01605 promotes tumor-infiltrating CD8 + T cell exhaustion and malignancy of clear cell renal cell carcinoma

doi: 10.3389/fimmu.2025.1744278

Figure Lengend Snippet: LINC01605 is associated with sialic acid levels and involved in JAK3/STAT3 signaling. (A, B) Uniform manifold approximation and projection (UMAP) plots of ccRCC samples and tumor-infiltrating CD8 + T cell subpopulation. (C) ccRCC samples with highly sialylated tumor cells had higher exhaustion scores and lower effector and cytotoxicity scores in the corresponding CD8 + T cell subpopulation. (D) Flow cytometry results indicated that LINC01605 silencing decreased sialic acid levels on the cell membrane of A498 and 786-O cell lines (n = 5 per group). (E) qRT-PCR and western blotting showed that LINC01605 expression was correlated with mRNA and protein expression of ST6GALNAC5 (n = 3 per group). (F) GSEA analysis in the TCGA-KIRC cohort (n=528) revealed that high LINC01605 expression was related to the IL6/JAK/STAT3 and MYC target pathways. (G) The mRNA expression of JAK3 and STAT3 was detected using qRT-PCR in LINC01605 -silenced ccRCC cell lines (n = 3 per group). (H) Western blotting was performed to detect the expression of JAK3, STAT3, phosphorylated STAT3, and downstream genes of the pathway after LINC01605 knockdown in ccRCC cell lines. (I) Binding sites of STAT3 at the ST6GALNAC5 promoter were predicted by JASPAR. (J) ChIP assays demonstrated that STAT3 bound to the ST6GALNAC5 promoter in A498 and 786-O cells (n = 3 per group). Values are presented as mean ± SD. P -values were calculated by two-tailed unpaired Student’s t-test (C, J) , one-way ANOVA followed Tukey’s multiple comparisons (D, E, G) , or non-parametric permutation test (F) . *p < 0.05; **p < 0.01; ***p < 0.001; ns, not significant. n represents the number of samples in (F) and the number of biological replicates in (D-E, G, J) .

Techniques: Flow Cytometry, Membrane, Quantitative RT-PCR, Western Blot, Expressing, Knockdown, Binding Assay, Two Tailed Test

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