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human luad cell lines pc9 (Procell Inc)

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Procell Inc human luad cell lines pc9

Upregulation of Hsp90α, Hsp90β, and EGFR expression in <t>LUAD</t> (A) Increased mRNA levels of Hsp90AA1, Hsp90AB1, and EGFR in tumors and adjacent tissues were obtained from the TCGA. (B) Increased protein levels of Hsp90α, Hsp90β, and EGFR in LUAD. (C) Positive correlations between Hsp90α and EGFR and between Hsp90β and EGFR. (D) Higher Hsp90α, Hsp90β, and EGFR levels were detected in the NSCLC cell lines <t>A549,</t> <t>NCI-H1299,</t> HCC827, <t>H358,</t> <t>PC9,</t> and H1975 than in the human normal lung epithelial cell line BEAS-2B. (E,F) qRT-PCR analyses showed increased mRNA expression. The band intensities were quantified by ImageJ v 1.8.0, and the data are presented as the mean±SD. n=3. ** P<0.01, *** P<0.001.

Human Luad Cell Lines Pc9, supplied by Procell Inc, 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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Average 90 stars, based on 1 article reviews

human luad cell lines pc9 - by Bioz Stars, 2026-03

90/100 stars

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1) Product Images from "Combined treatment with cetuximab and STA9090 has synergistic anticancer effects on human non-small cell lung cancer"

Article Title: Combined treatment with cetuximab and STA9090 has synergistic anticancer effects on human non-small cell lung cancer

Journal: Acta Biochimica et Biophysica Sinica

doi: 10.3724/abbs.2024069

Upregulation of Hsp90α, Hsp90β, and EGFR expression in LUAD (A) Increased mRNA levels of Hsp90AA1, Hsp90AB1, and EGFR in tumors and adjacent tissues were obtained from the TCGA. (B) Increased protein levels of Hsp90α, Hsp90β, and EGFR in LUAD. (C) Positive correlations between Hsp90α and EGFR and between Hsp90β and EGFR. (D) Higher Hsp90α, Hsp90β, and EGFR levels were detected in the NSCLC cell lines A549, NCI-H1299, HCC827, H358, PC9, and H1975 than in the human normal lung epithelial cell line BEAS-2B. (E,F) qRT-PCR analyses showed increased mRNA expression. The band intensities were quantified by ImageJ v 1.8.0, and the data are presented as the mean±SD. n=3. ** P<0.01, *** P<0.001.

Figure Legend Snippet: Upregulation of Hsp90α, Hsp90β, and EGFR expression in LUAD (A) Increased mRNA levels of Hsp90AA1, Hsp90AB1, and EGFR in tumors and adjacent tissues were obtained from the TCGA. (B) Increased protein levels of Hsp90α, Hsp90β, and EGFR in LUAD. (C) Positive correlations between Hsp90α and EGFR and between Hsp90β and EGFR. (D) Higher Hsp90α, Hsp90β, and EGFR levels were detected in the NSCLC cell lines A549, NCI-H1299, HCC827, H358, PC9, and H1975 than in the human normal lung epithelial cell line BEAS-2B. (E,F) qRT-PCR analyses showed increased mRNA expression. The band intensities were quantified by ImageJ v 1.8.0, and the data are presented as the mean±SD. n=3. ** P<0.01, *** P<0.001.

Techniques Used: Expressing, Quantitative RT-PCR

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Journal: Acta Biochimica et Biophysica Sinica

Article Title: Combined treatment with cetuximab and STA9090 has synergistic anticancer effects on human non-small cell lung cancer

doi: 10.3724/abbs.2024069

Figure Lengend Snippet: Upregulation of Hsp90α, Hsp90β, and EGFR expression in LUAD (A) Increased mRNA levels of Hsp90AA1, Hsp90AB1, and EGFR in tumors and adjacent tissues were obtained from the TCGA. (B) Increased protein levels of Hsp90α, Hsp90β, and EGFR in LUAD. (C) Positive correlations between Hsp90α and EGFR and between Hsp90β and EGFR. (D) Higher Hsp90α, Hsp90β, and EGFR levels were detected in the NSCLC cell lines A549, NCI-H1299, HCC827, H358, PC9, and H1975 than in the human normal lung epithelial cell line BEAS-2B. (E,F) qRT-PCR analyses showed increased mRNA expression. The band intensities were quantified by ImageJ v 1.8.0, and the data are presented as the mean±SD. n=3. ** P<0.01, *** P<0.001.

Article Snippet: Human LUAD cell lines (PC9 , A549, H827, H358, PC9 and NCI-H1299) and lung epithelial cell line BEAS-2B were obtained from Procell Life Science & Technology Co., Ltd (Wuhan, China).

Techniques: Expressing, Quantitative RT-PCR

Upregulated MCF2L-AS1 promotes LUAD cell growth and cisplatin resistance. (A) The expression level of MCF2L-AS1 in human normal lung epithelial cell line (BEAS-2B) and LUAD cell lines (PC9, HCC827, A549 and NCI–H23). (B) The knockdown efficiency of sh-MCF2L-AS1#1/2 in LIAD cells. (C–E) Cell proliferation was evaluated in sh-MCF2L-AS1 transfected cells by performing CCK-8, colony formation and EdU assays. (F–G) Caspase-3 activity assay and TUNEL assay were carried out to examine cell apoptosis in LUAD MCF2L-AS1 silenced LUAD cells. (H) The migration of LUAD cells was tested with Western blot assay upon MCF2L-AS1 depletion. (I) Transwell assay was conducted to assess the invasion in LUAD cells transfected with sh-MCF2L-AS1. (J) The effect of MCF2L-AS1 knockdown on cell viability in cisplatin treated LUAD cells was measured with MTT assay. **P < 0.01.

Journal: Heliyon

Article Title: MCF2L-AS1/miR-874-3p/STAT3 feedback loop contributes to lung adenocarcinoma cell growth and cisplatin resistance

doi: 10.1016/j.heliyon.2023.e21342

Figure Lengend Snippet: Upregulated MCF2L-AS1 promotes LUAD cell growth and cisplatin resistance. (A) The expression level of MCF2L-AS1 in human normal lung epithelial cell line (BEAS-2B) and LUAD cell lines (PC9, HCC827, A549 and NCI–H23). (B) The knockdown efficiency of sh-MCF2L-AS1#1/2 in LIAD cells. (C–E) Cell proliferation was evaluated in sh-MCF2L-AS1 transfected cells by performing CCK-8, colony formation and EdU assays. (F–G) Caspase-3 activity assay and TUNEL assay were carried out to examine cell apoptosis in LUAD MCF2L-AS1 silenced LUAD cells. (H) The migration of LUAD cells was tested with Western blot assay upon MCF2L-AS1 depletion. (I) Transwell assay was conducted to assess the invasion in LUAD cells transfected with sh-MCF2L-AS1. (J) The effect of MCF2L-AS1 knockdown on cell viability in cisplatin treated LUAD cells was measured with MTT assay. **P < 0.01.

Article Snippet: In addition, the LUAD cell line PC9 was sourced from Procell Life Science & Technology (Wuhan, China).

Techniques: Expressing, Knockdown, Transfection, CCK-8 Assay, Caspase-3 Activity Assay, TUNEL Assay, Migration, Western Blot, Transwell Assay, MTT Assay

$MCF2L-AS1 sponges miR-874-3p in LUAD. (A–B) Subcellular fractionation and FISH assays were used to determine the distribution of MCF2L-AS1 in LUAD cells. (C) The predicted miRNAs for MCF2L-AS1 from starBase. (D) The expressions of potential miRNAs in LUAD cells. (E) MiR-874-3p expression in human normal lung epithelial cell line (BEAS-2B) and LUAD cell lines (PC9, HCC827, A549 and NCI–H23). (F) The expression level of miR-874-3p in sh-MCF2L-AS1 transfected cells. (G) RIP assay was applied to evaluate the interaction between MCF2L-AS1 and miR-874-3p. (H) The binding site between MCF2L-AS1 and miR-874-3p. (I) Transfection efficiency of miR-874-3p mimics was tested in LUAD cells. (J) Luciferase reporter assay was employed to further confirm the combination of miR-874-3p in MCF2L-AS1. **P < 0.01.$

Journal: Heliyon

Article Title: MCF2L-AS1/miR-874-3p/STAT3 feedback loop contributes to lung adenocarcinoma cell growth and cisplatin resistance

doi: 10.1016/j.heliyon.2023.e21342

Figure Lengend Snippet: MCF2L-AS1 sponges miR-874-3p in LUAD. (A–B) Subcellular fractionation and FISH assays were used to determine the distribution of MCF2L-AS1 in LUAD cells. (C) The predicted miRNAs for MCF2L-AS1 from starBase. (D) The expressions of potential miRNAs in LUAD cells. (E) MiR-874-3p expression in human normal lung epithelial cell line (BEAS-2B) and LUAD cell lines (PC9, HCC827, A549 and NCI–H23). (F) The expression level of miR-874-3p in sh-MCF2L-AS1 transfected cells. (G) RIP assay was applied to evaluate the interaction between MCF2L-AS1 and miR-874-3p. (H) The binding site between MCF2L-AS1 and miR-874-3p. (I) Transfection efficiency of miR-874-3p mimics was tested in LUAD cells. (J) Luciferase reporter assay was employed to further confirm the combination of miR-874-3p in MCF2L-AS1. **P < 0.01.

Article Snippet: In addition, the LUAD cell line PC9 was sourced from Procell Life Science & Technology (Wuhan, China).

Techniques: Fractionation, Expressing, Transfection, Binding Assay, Luciferase, Reporter Assay

STAT3 is a target of miR-874-3p. (A) Potential target mRNAs of miR-874-3p predicted by PITA, PicTar, miRanda, microT and miRmap. (B) Underlying downstream mRNAs that could be upregulated in LUAD cells and downregulated by miR-874-3p mimics. (C) RNA pull-down assay was utilized to examine the enrichment of STAT3, TRIB2 and SLC12A5 in miR-874-3p biotin probe. (D) The expression of STAT3 in human normal lung epithelial cell line (BEAS-2B) and LUAD cell lines (PC9, HCC827, A549 and NCI–H23). (E) The interaction between miR-874-3p together with MCF2L-AS1 and STAT3 was determined by RIP assay. (F) The potential binding site between miR-874-3p and STAT3 was predicted through starBase. (G) MiR-874-3p was verified to combine with STAT3 through luciferase reporter assay. (H–I) STAT3 mRNA and protein levels were assessed in LUAD cells transfected with miR-874-3p mimics. (J–K) qRT-PCR and Western blot assays were employed to detect the mRNA and protein levels of STAT3 in MCF2L-AS1 downregulated LUAD cells. **P < 0.01.

Journal: Heliyon

Article Title: MCF2L-AS1/miR-874-3p/STAT3 feedback loop contributes to lung adenocarcinoma cell growth and cisplatin resistance

doi: 10.1016/j.heliyon.2023.e21342

Figure Lengend Snippet: STAT3 is a target of miR-874-3p. (A) Potential target mRNAs of miR-874-3p predicted by PITA, PicTar, miRanda, microT and miRmap. (B) Underlying downstream mRNAs that could be upregulated in LUAD cells and downregulated by miR-874-3p mimics. (C) RNA pull-down assay was utilized to examine the enrichment of STAT3, TRIB2 and SLC12A5 in miR-874-3p biotin probe. (D) The expression of STAT3 in human normal lung epithelial cell line (BEAS-2B) and LUAD cell lines (PC9, HCC827, A549 and NCI–H23). (E) The interaction between miR-874-3p together with MCF2L-AS1 and STAT3 was determined by RIP assay. (F) The potential binding site between miR-874-3p and STAT3 was predicted through starBase. (G) MiR-874-3p was verified to combine with STAT3 through luciferase reporter assay. (H–I) STAT3 mRNA and protein levels were assessed in LUAD cells transfected with miR-874-3p mimics. (J–K) qRT-PCR and Western blot assays were employed to detect the mRNA and protein levels of STAT3 in MCF2L-AS1 downregulated LUAD cells. **P < 0.01.

Article Snippet: In addition, the LUAD cell line PC9 was sourced from Procell Life Science & Technology (Wuhan, China).

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

MCF2L-AS1 facilitate LUAD cell growth by targeting miR-874-3p/STAT3. (A) Expressions of miR-874-3p and STAT3 were tested by separately transfecting miR-874-3p inhibitor and sh-STAT3. (B–D) The proliferative capacity of MCF2L-AS1 silenced cells was estimated after transfecting NC inhibitor, miR-874-3p inhibitor, miR-874-3p inhibitor plus sh-STAT3. (E–F) NC inhibitor, miR-874-3p inhibitor, miR-874-3p inhibitor plus sh-STAT3 were transfected into MCF2L-AS1 downregulated cells to observe cell apoptosis. (G) Cell migration was evaluated after transfecting above appointed plasmids in sh-MCF2L-AS1 transfected cells. (H) Above appointed plasmids were transfected into MCF2L-AS1 downregulated cells to detect cell invasion. **P < 0.01.

Journal: Heliyon

Article Title: MCF2L-AS1/miR-874-3p/STAT3 feedback loop contributes to lung adenocarcinoma cell growth and cisplatin resistance

doi: 10.1016/j.heliyon.2023.e21342

Figure Lengend Snippet: MCF2L-AS1 facilitate LUAD cell growth by targeting miR-874-3p/STAT3. (A) Expressions of miR-874-3p and STAT3 were tested by separately transfecting miR-874-3p inhibitor and sh-STAT3. (B–D) The proliferative capacity of MCF2L-AS1 silenced cells was estimated after transfecting NC inhibitor, miR-874-3p inhibitor, miR-874-3p inhibitor plus sh-STAT3. (E–F) NC inhibitor, miR-874-3p inhibitor, miR-874-3p inhibitor plus sh-STAT3 were transfected into MCF2L-AS1 downregulated cells to observe cell apoptosis. (G) Cell migration was evaluated after transfecting above appointed plasmids in sh-MCF2L-AS1 transfected cells. (H) Above appointed plasmids were transfected into MCF2L-AS1 downregulated cells to detect cell invasion. **P < 0.01.

Article Snippet: In addition, the LUAD cell line PC9 was sourced from Procell Life Science & Technology (Wuhan, China).

Techniques: Transfection, Migration

STAT3 binds to MCF2L-AS1 promoter. (A–B) The overexpression efficiency of STAT3 was detected in LUAD cells. (C) MCF2L-AS1 expression in STAT3 overexpressed LUAD cells. (D) The effect of STAT3 knockdown on MCF2L-AS1 expression. (E) The binding sites between STAT3 and MCF2L-AS1 promoter. (F) ChIP assay was performed to determine the interaction between STAT3 and MCF2L-AS1 promoter. (G) Luciferase reporter assay was utilized to measure the combination of STAT3 in MCF2L-AS1 promoter. **P < 0.01.

Journal: Heliyon

Article Title: MCF2L-AS1/miR-874-3p/STAT3 feedback loop contributes to lung adenocarcinoma cell growth and cisplatin resistance

doi: 10.1016/j.heliyon.2023.e21342

Figure Lengend Snippet: STAT3 binds to MCF2L-AS1 promoter. (A–B) The overexpression efficiency of STAT3 was detected in LUAD cells. (C) MCF2L-AS1 expression in STAT3 overexpressed LUAD cells. (D) The effect of STAT3 knockdown on MCF2L-AS1 expression. (E) The binding sites between STAT3 and MCF2L-AS1 promoter. (F) ChIP assay was performed to determine the interaction between STAT3 and MCF2L-AS1 promoter. (G) Luciferase reporter assay was utilized to measure the combination of STAT3 in MCF2L-AS1 promoter. **P < 0.01.

Article Snippet: In addition, the LUAD cell line PC9 was sourced from Procell Life Science & Technology (Wuhan, China).

Techniques: Over Expression, Expressing, Knockdown, Binding Assay, Luciferase, Reporter Assay

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