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luad cell lines (nci-h1975; nci-h441; pc-9; a549)  (Shanghai iCELL Biotechnology Co Ltd)
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Shanghai iCELL Biotechnology Co Ltd luad cell lines (nci-h1975; nci-h441; pc-9; a549)
Upregulated LINC00511 accelerated tumorigenesis in <t>LUAD.</t> (a) LINC00511 expression is up-regulated in tumor samples than in the normal samples in TCGA data by GEPIA webtool. (b-c) OS (b) and RFS (c) in LUAD. OS: overall survival; RFS: disease-free survival. (d) LINC00511 expression in LUAD cell lines. (e) Transfection of si-NC or si-LINC00511 to PC-9 <t>and</t> <t>A549</t> cell. LINC00511 downregulations in two LUAD cell lines via si-LINC00511 treatment were realized. (f-g) Cell viability of PC-9 (f) and A549 (g) cells with or without si-LINC00511 treatment. LUAD cell viability was suppressed after LINC00511 expression being inhibited. (h) Colony formation of PC-9 and A549 cells treated with si-NC or si-LINC00511. The colony number in LINC00511-transfected LUAD cells was less than negative control group. (i) Flow cytometry results indicate an upregulation of LUAD cells apoptosis occurred when LINC00511 expression was blocked. * P < .05, ** P < .01, compared with the normal group or si-NC group.
Luad Cell Lines (Nci H1975; Nci H441; Pc 9; A549), supplied by Shanghai iCELL Biotechnology Co Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Upregulated LINC00511 accelerated tumorigenesis in LUAD. (a) LINC00511 expression is up-regulated in tumor samples than in the normal samples in TCGA data by GEPIA webtool. (b-c) OS (b) and RFS (c) in LUAD. OS: overall survival; RFS: disease-free survival. (d) LINC00511 expression in LUAD cell lines. (e) Transfection of si-NC or si-LINC00511 to PC-9 and A549 cell. LINC00511 downregulations in two LUAD cell lines via si-LINC00511 treatment were realized. (f-g) Cell viability of PC-9 (f) and A549 (g) cells with or without si-LINC00511 treatment. LUAD cell viability was suppressed after LINC00511 expression being inhibited. (h) Colony formation of PC-9 and A549 cells treated with si-NC or si-LINC00511. The colony number in LINC00511-transfected LUAD cells was less than negative control group. (i) Flow cytometry results indicate an upregulation of LUAD cells apoptosis occurred when LINC00511 expression was blocked. * P < .05, ** P < .01, compared with the normal group or si-NC group.

Journal: Cancer Biology & Therapy

Article Title: Knockdown of LINC00511 enhances radiosensitivity of lung adenocarcinoma via regulating miR-497-5p/SMAD3

doi: 10.1080/15384047.2023.2165896

Figure Lengend Snippet: Upregulated LINC00511 accelerated tumorigenesis in LUAD. (a) LINC00511 expression is up-regulated in tumor samples than in the normal samples in TCGA data by GEPIA webtool. (b-c) OS (b) and RFS (c) in LUAD. OS: overall survival; RFS: disease-free survival. (d) LINC00511 expression in LUAD cell lines. (e) Transfection of si-NC or si-LINC00511 to PC-9 and A549 cell. LINC00511 downregulations in two LUAD cell lines via si-LINC00511 treatment were realized. (f-g) Cell viability of PC-9 (f) and A549 (g) cells with or without si-LINC00511 treatment. LUAD cell viability was suppressed after LINC00511 expression being inhibited. (h) Colony formation of PC-9 and A549 cells treated with si-NC or si-LINC00511. The colony number in LINC00511-transfected LUAD cells was less than negative control group. (i) Flow cytometry results indicate an upregulation of LUAD cells apoptosis occurred when LINC00511 expression was blocked. * P < .05, ** P < .01, compared with the normal group or si-NC group.

Article Snippet: Human normal lung epithelial cell-line BEAS-2B and 4 LUAD cell lines (NCI-H1975; NCI-H441; PC-9; A549) were obtained from Shanghai iCell Bioscience Inc. BEAS-2B were seeded in DMEM medium supplemented with 10% fetal bovine serum (FBS, Gibco, Waltham, MA) and 1% Pen/Strep solution.

Techniques: Expressing, Transfection, Negative Control, Flow Cytometry

Upregulated LINC00511 in LUAD cells after irradiation treatment. (a) 24 h later, LINC00511 expression in PC-9 and A549 cells treated with different doses of IR was detected by qRT-PCR. (b) LINC00511 expression in PC-9 and A549 cells treated with 4 Gy IR was detected every 4 hours for 24 hours by qRT-PCR. ** P < .01, compared with 0 Gy group.

Journal: Cancer Biology & Therapy

Article Title: Knockdown of LINC00511 enhances radiosensitivity of lung adenocarcinoma via regulating miR-497-5p/SMAD3

doi: 10.1080/15384047.2023.2165896

Figure Lengend Snippet: Upregulated LINC00511 in LUAD cells after irradiation treatment. (a) 24 h later, LINC00511 expression in PC-9 and A549 cells treated with different doses of IR was detected by qRT-PCR. (b) LINC00511 expression in PC-9 and A549 cells treated with 4 Gy IR was detected every 4 hours for 24 hours by qRT-PCR. ** P < .01, compared with 0 Gy group.

Article Snippet: Human normal lung epithelial cell-line BEAS-2B and 4 LUAD cell lines (NCI-H1975; NCI-H441; PC-9; A549) were obtained from Shanghai iCell Bioscience Inc. BEAS-2B were seeded in DMEM medium supplemented with 10% fetal bovine serum (FBS, Gibco, Waltham, MA) and 1% Pen/Strep solution.

Techniques: Irradiation, Expressing, Quantitative RT-PCR

LINC00511 knockdown potentiated radiosensitivity of LUAD cells. (a) Survival fraction of PC-9 and A549 cells exposed to gradient dose of radiation. LUAD cell survival stepped down along with the radiation dose rising. (b) Survival fraction of PC-9 and A549 cells at different LINC00511 levels under gradient IR. The decline of LUAD cell survival via radiation treatment intensified further when LINC00511 expression was blocked. (c) Cell viability of PC-9 and A549 cells under different treatments. Radiation treatment and si-LINC00511 both decreased cell viability in two cell lines. And the combination of radiation treatment and si-LINC00511 transfection further inhibited LUAD cell viability compared to the groups with single treatment. (d) Colony formation of PC-9 and A549 cells in different groups. Colony numbers in si-LINC00511 group as well as si-NC+4 Gy radiation group were both smaller than the normal control. Si-LINC00511 + 4 Gy radiation presented additional suppression in colony formation. (e) Apoptosis rate of PC-9 and A549 cells with different treatments. Based on the flow cytometry, the apoptosis was activated in si-LINC00511-transfected or radiation-treated LUAD cells. In the group treated with si-LINC00511 and 4 Gy radiation, the apoptosis activation was further promoted. (f) γ-H2AX staining of PC-9 and A549 cells under different treatments. Cells treated by si-LINC00511 exhibited enhanced DNA damage in malignant cells treated by radiation. * P < .05, ** P < .01.

Journal: Cancer Biology & Therapy

Article Title: Knockdown of LINC00511 enhances radiosensitivity of lung adenocarcinoma via regulating miR-497-5p/SMAD3

doi: 10.1080/15384047.2023.2165896

Figure Lengend Snippet: LINC00511 knockdown potentiated radiosensitivity of LUAD cells. (a) Survival fraction of PC-9 and A549 cells exposed to gradient dose of radiation. LUAD cell survival stepped down along with the radiation dose rising. (b) Survival fraction of PC-9 and A549 cells at different LINC00511 levels under gradient IR. The decline of LUAD cell survival via radiation treatment intensified further when LINC00511 expression was blocked. (c) Cell viability of PC-9 and A549 cells under different treatments. Radiation treatment and si-LINC00511 both decreased cell viability in two cell lines. And the combination of radiation treatment and si-LINC00511 transfection further inhibited LUAD cell viability compared to the groups with single treatment. (d) Colony formation of PC-9 and A549 cells in different groups. Colony numbers in si-LINC00511 group as well as si-NC+4 Gy radiation group were both smaller than the normal control. Si-LINC00511 + 4 Gy radiation presented additional suppression in colony formation. (e) Apoptosis rate of PC-9 and A549 cells with different treatments. Based on the flow cytometry, the apoptosis was activated in si-LINC00511-transfected or radiation-treated LUAD cells. In the group treated with si-LINC00511 and 4 Gy radiation, the apoptosis activation was further promoted. (f) γ-H2AX staining of PC-9 and A549 cells under different treatments. Cells treated by si-LINC00511 exhibited enhanced DNA damage in malignant cells treated by radiation. * P < .05, ** P < .01.

Article Snippet: Human normal lung epithelial cell-line BEAS-2B and 4 LUAD cell lines (NCI-H1975; NCI-H441; PC-9; A549) were obtained from Shanghai iCell Bioscience Inc. BEAS-2B were seeded in DMEM medium supplemented with 10% fetal bovine serum (FBS, Gibco, Waltham, MA) and 1% Pen/Strep solution.

Techniques: Knockdown, Expressing, Transfection, Control, Flow Cytometry, Activation Assay, Staining

Cytoplasmic LINC00511 was an endogenous sponge of miR-497-5p in LUAD. (a) LINC00511 information in lncATLAS. LINC00511 was predicted to locate in cytoplasm. (b) Subcellular location of LINC00511. Both in PC-9 and A549 cells, LINC00511 was identified to be located in cytoplasm. (c) Targeting relationship between LINC00511 and miR-497-5p. miR-497-5p was predicted binding to LINC00511. (d) Transfection of miR-NC or miR-497-5p to PC-9 and A549 cells. miR-497-5p expression was successfully upregulated in two LUAD cell lines after transfection. (e) Luciferase assays in PC-9 and A549. (f) LINC00511 enrichment in PC-9 and A549. Luciferase assays and miRNA array testing both proved miR-497-5p binds to LINC00511. (g) miR-497-5p expression in LUAD cell lines. (h) miR-497-5p expression in PC-9 and A549 cells treated with 4 Gy IR was detected every 4 hours for 24 hours by qRT-PCR. (i) MiR-497-5p expression in PC-9 and A549 cells transfected with si-NC or si-LINC00511. LINC00511 upregulation in LUAD cells inhibited miR-497-5p expression. ** P < .01, compared with the NC group or 0 Gy group.

Journal: Cancer Biology & Therapy

Article Title: Knockdown of LINC00511 enhances radiosensitivity of lung adenocarcinoma via regulating miR-497-5p/SMAD3

doi: 10.1080/15384047.2023.2165896

Figure Lengend Snippet: Cytoplasmic LINC00511 was an endogenous sponge of miR-497-5p in LUAD. (a) LINC00511 information in lncATLAS. LINC00511 was predicted to locate in cytoplasm. (b) Subcellular location of LINC00511. Both in PC-9 and A549 cells, LINC00511 was identified to be located in cytoplasm. (c) Targeting relationship between LINC00511 and miR-497-5p. miR-497-5p was predicted binding to LINC00511. (d) Transfection of miR-NC or miR-497-5p to PC-9 and A549 cells. miR-497-5p expression was successfully upregulated in two LUAD cell lines after transfection. (e) Luciferase assays in PC-9 and A549. (f) LINC00511 enrichment in PC-9 and A549. Luciferase assays and miRNA array testing both proved miR-497-5p binds to LINC00511. (g) miR-497-5p expression in LUAD cell lines. (h) miR-497-5p expression in PC-9 and A549 cells treated with 4 Gy IR was detected every 4 hours for 24 hours by qRT-PCR. (i) MiR-497-5p expression in PC-9 and A549 cells transfected with si-NC or si-LINC00511. LINC00511 upregulation in LUAD cells inhibited miR-497-5p expression. ** P < .01, compared with the NC group or 0 Gy group.

Article Snippet: Human normal lung epithelial cell-line BEAS-2B and 4 LUAD cell lines (NCI-H1975; NCI-H441; PC-9; A549) were obtained from Shanghai iCell Bioscience Inc. BEAS-2B were seeded in DMEM medium supplemented with 10% fetal bovine serum (FBS, Gibco, Waltham, MA) and 1% Pen/Strep solution.

Techniques: Binding Assay, Transfection, Expressing, Luciferase, Quantitative RT-PCR

miR-497-5p overexpression promoted the radiosensitivity of LUAD cells. (a) Cell viability of PC-9 and A549 cells under different treatments. Radiation treatment and miR-497-5p both decreased cell viability in two cell lines. The combination of radiation treatment and miR-497-5p transfection further inhibited PC-9 and A549 cells viability compared to the groups with single treatment. (b-c) Colony formation of PC-9 and A549 cells in different groups. Colony numbers in miR-497-5p or 4 Gy radiation treated LUAD cells were both lower than the normal control. And the miR-497-5p+4 Gy radiation presented additional suppression in colony formation. (d-e) Apoptosis rate of PC-9 and A549 cells with different treatments. Flow cytometry results reveal that the apoptosis was activated in miR-497-5p group or 4 Gy radiation group. In miR-497-5p+4 Gy radiation group, apoptosis activation was further enhanced. * P < .05, ** P < .01.

Journal: Cancer Biology & Therapy

Article Title: Knockdown of LINC00511 enhances radiosensitivity of lung adenocarcinoma via regulating miR-497-5p/SMAD3

doi: 10.1080/15384047.2023.2165896

Figure Lengend Snippet: miR-497-5p overexpression promoted the radiosensitivity of LUAD cells. (a) Cell viability of PC-9 and A549 cells under different treatments. Radiation treatment and miR-497-5p both decreased cell viability in two cell lines. The combination of radiation treatment and miR-497-5p transfection further inhibited PC-9 and A549 cells viability compared to the groups with single treatment. (b-c) Colony formation of PC-9 and A549 cells in different groups. Colony numbers in miR-497-5p or 4 Gy radiation treated LUAD cells were both lower than the normal control. And the miR-497-5p+4 Gy radiation presented additional suppression in colony formation. (d-e) Apoptosis rate of PC-9 and A549 cells with different treatments. Flow cytometry results reveal that the apoptosis was activated in miR-497-5p group or 4 Gy radiation group. In miR-497-5p+4 Gy radiation group, apoptosis activation was further enhanced. * P < .05, ** P < .01.

Article Snippet: Human normal lung epithelial cell-line BEAS-2B and 4 LUAD cell lines (NCI-H1975; NCI-H441; PC-9; A549) were obtained from Shanghai iCell Bioscience Inc. BEAS-2B were seeded in DMEM medium supplemented with 10% fetal bovine serum (FBS, Gibco, Waltham, MA) and 1% Pen/Strep solution.

Techniques: Over Expression, Transfection, Control, Flow Cytometry, Activation Assay

LINC00511 regulated SMAD3 expression via miR-497-5p. (a) Targeting relationship between miR-497-5p and SMAD3. (b) Luciferase assays in PC-9 and A549 cells. SMAD3 binding to miR-497-5p was confirmed in LUAD cells. (c) SMAD3 expression in LUAD cell lines. (d) SMAD3 expression in PC-9 and A549 cells treated with 4 Gy IR was detected every 4 hours for 24 hours by qRT-PCR. (e) 24 hours later, SMAD3 expression in PC-9 and A549 cells treated with 4 Gy IR was detected by western blot. (f-g) 48 hours later, the mRNA (f) and protein (g) level of SMAD3 in PC-9 and A549 cells transfected with si-LINC00511 was detected by qRT-PCR and western blot. (h-i) 48 hours later, the mRNA (h) and protein (i) level of SMAD3 in PC-9 and A549 cells transfected with miR-497-5p mimics was detected by qRT-PCR and western blot. * P < .05, ** P < .01, compared with the NC group.

Journal: Cancer Biology & Therapy

Article Title: Knockdown of LINC00511 enhances radiosensitivity of lung adenocarcinoma via regulating miR-497-5p/SMAD3

doi: 10.1080/15384047.2023.2165896

Figure Lengend Snippet: LINC00511 regulated SMAD3 expression via miR-497-5p. (a) Targeting relationship between miR-497-5p and SMAD3. (b) Luciferase assays in PC-9 and A549 cells. SMAD3 binding to miR-497-5p was confirmed in LUAD cells. (c) SMAD3 expression in LUAD cell lines. (d) SMAD3 expression in PC-9 and A549 cells treated with 4 Gy IR was detected every 4 hours for 24 hours by qRT-PCR. (e) 24 hours later, SMAD3 expression in PC-9 and A549 cells treated with 4 Gy IR was detected by western blot. (f-g) 48 hours later, the mRNA (f) and protein (g) level of SMAD3 in PC-9 and A549 cells transfected with si-LINC00511 was detected by qRT-PCR and western blot. (h-i) 48 hours later, the mRNA (h) and protein (i) level of SMAD3 in PC-9 and A549 cells transfected with miR-497-5p mimics was detected by qRT-PCR and western blot. * P < .05, ** P < .01, compared with the NC group.

Article Snippet: Human normal lung epithelial cell-line BEAS-2B and 4 LUAD cell lines (NCI-H1975; NCI-H441; PC-9; A549) were obtained from Shanghai iCell Bioscience Inc. BEAS-2B were seeded in DMEM medium supplemented with 10% fetal bovine serum (FBS, Gibco, Waltham, MA) and 1% Pen/Strep solution.

Techniques: Expressing, Luciferase, Binding Assay, Quantitative RT-PCR, Western Blot, Transfection

SMAD3 suppression enhanced the radiosensitivity of LUAD cells. (a) SMAD3 mRNA expression in PC-9 and A549 cells treated with si-NC or si-SMAD3. (b) Western blot of SMAD3 in cells with or without si-SMAD3 treatment. (c) PC-9 and A549 cells’ survival fraction at different SMAD3 levels under gradient radiation treatment. The decline of LUAD cell survival via radiation dose rising was expanded after SMAD3 downregulation. (d-e) Apoptosis rate of PC-9 and A549 cells under different treatments. In accordance with flow cytometry results, apoptosis was activated in si-SMAD3-transfected or 4 Gy radiation-treated LUAD cells. In the group treated with the combination of si-SMAD3 and 4 Gy radiation, cell apoptosis was further promoted. ** P < .01, compared with the NC group.

Journal: Cancer Biology & Therapy

Article Title: Knockdown of LINC00511 enhances radiosensitivity of lung adenocarcinoma via regulating miR-497-5p/SMAD3

doi: 10.1080/15384047.2023.2165896

Figure Lengend Snippet: SMAD3 suppression enhanced the radiosensitivity of LUAD cells. (a) SMAD3 mRNA expression in PC-9 and A549 cells treated with si-NC or si-SMAD3. (b) Western blot of SMAD3 in cells with or without si-SMAD3 treatment. (c) PC-9 and A549 cells’ survival fraction at different SMAD3 levels under gradient radiation treatment. The decline of LUAD cell survival via radiation dose rising was expanded after SMAD3 downregulation. (d-e) Apoptosis rate of PC-9 and A549 cells under different treatments. In accordance with flow cytometry results, apoptosis was activated in si-SMAD3-transfected or 4 Gy radiation-treated LUAD cells. In the group treated with the combination of si-SMAD3 and 4 Gy radiation, cell apoptosis was further promoted. ** P < .01, compared with the NC group.

Article Snippet: Human normal lung epithelial cell-line BEAS-2B and 4 LUAD cell lines (NCI-H1975; NCI-H441; PC-9; A549) were obtained from Shanghai iCell Bioscience Inc. BEAS-2B were seeded in DMEM medium supplemented with 10% fetal bovine serum (FBS, Gibco, Waltham, MA) and 1% Pen/Strep solution.

Techniques: Expressing, Western Blot, Flow Cytometry, Transfection

LINC00511 inhibition activated miR-497-5p and mediately downregulated SMAD3, which further promoted radiosensitivity in LUAD cells. (a) SMAD3 mRNA expression in PC-9 and A549 cells of different groups. (b) SMAD3 protein expression in PC-9 and A549 cells with different treatments. Compared to the NC, si-LINC00511 transfection induced a sharp decline in SMAD3 expression, which was reversed with additional anti-miR-497-5p or SMAD3 treatment. (c) Cell viability of 4 Gy radiation-treated PC-9 and A549 cells with different treatments. Downregulated LINC00511 decreased LUAD cell viability, and along with the prolonged radiation time the decreasing was more significant, which was reversed with miR-497-5p inhibition or SMAD3 activation. (d) Colony formation of 4 Gy radiation-treated PC-9 and A549 cells with different treatments. LINC00511 downregulation suppressed colony formation of IR-treated LUAD cells while additional miR-497-5p inhibition or SMAD3 activation reactivated it. (e) Apoptosis rate of 4 Gy radiation-treated PC-9 and A549 cells in different groups. 4 Gy radiation-triggered apoptosis was further promoted via si-LINC00511 transfection, which was repressed with additional anti-miR-497-5p or SMAD3 treatment. ** P < .01, compared with the NC group.

Journal: Cancer Biology & Therapy

Article Title: Knockdown of LINC00511 enhances radiosensitivity of lung adenocarcinoma via regulating miR-497-5p/SMAD3

doi: 10.1080/15384047.2023.2165896

Figure Lengend Snippet: LINC00511 inhibition activated miR-497-5p and mediately downregulated SMAD3, which further promoted radiosensitivity in LUAD cells. (a) SMAD3 mRNA expression in PC-9 and A549 cells of different groups. (b) SMAD3 protein expression in PC-9 and A549 cells with different treatments. Compared to the NC, si-LINC00511 transfection induced a sharp decline in SMAD3 expression, which was reversed with additional anti-miR-497-5p or SMAD3 treatment. (c) Cell viability of 4 Gy radiation-treated PC-9 and A549 cells with different treatments. Downregulated LINC00511 decreased LUAD cell viability, and along with the prolonged radiation time the decreasing was more significant, which was reversed with miR-497-5p inhibition or SMAD3 activation. (d) Colony formation of 4 Gy radiation-treated PC-9 and A549 cells with different treatments. LINC00511 downregulation suppressed colony formation of IR-treated LUAD cells while additional miR-497-5p inhibition or SMAD3 activation reactivated it. (e) Apoptosis rate of 4 Gy radiation-treated PC-9 and A549 cells in different groups. 4 Gy radiation-triggered apoptosis was further promoted via si-LINC00511 transfection, which was repressed with additional anti-miR-497-5p or SMAD3 treatment. ** P < .01, compared with the NC group.

Article Snippet: Human normal lung epithelial cell-line BEAS-2B and 4 LUAD cell lines (NCI-H1975; NCI-H441; PC-9; A549) were obtained from Shanghai iCell Bioscience Inc. BEAS-2B were seeded in DMEM medium supplemented with 10% fetal bovine serum (FBS, Gibco, Waltham, MA) and 1% Pen/Strep solution.

Techniques: Inhibition, Expressing, Transfection, Activation Assay