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Becton Dickinson quick-diff stain kit
Quick Diff Stain Kit, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/diff-quick+kit/quick+diff+stain+kit/pm10766865-58-27-30
Average 90 stars, based on 1 article reviews
quick-diff stain kit - by Bioz Stars, 2026-09
90/100 stars

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Related Articles

Membrane:

Article Title: Prostaglandin E 2 stimulates urokinase-type plasminogen activator receptor via EP2 receptor-dependent signaling pathways in human AGS gastric cancer cells.
Article Snippet: This article is protected by copyright.. All rights reserved 2 Aberrant expression of urokinase-type plasminogen activator receptor (uPAR) has been observed in human gastric cancers.. Prostaglandin E2 (PGE2), whose biosynthesis is catalyzed by cyclooxygenase-2 (COX-2), is implicated in cancer metastasis; however, the cellular and molecular mechanisms of PGE2-driven uPAR expression are yet to be elucidated in human gastric cancer AGS cells.

Article Title: Docosahexaenoic Acid Inhibits Tumor Promoter-Induced Urokinase-Type Plasminogen Activator Receptor by Suppressing PKCδ- and MAPKs-Mediated Pathways in ECV304 Human Endothelial Cells
Article Snippet: The non-invading cells on the upper surface of each membrane were removed from the chamber by using cotton swabs, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Sulforaphane Suppresses the Nicotine-Induced Expression of the Matrix Metalloproteinase-9 via Inhibiting ROS-Mediated AP-1 and NF-κB Signaling in Human Gastric Cancer Cells
Article Snippet: Briefly, AGS cells were added to the upper chamber with nicotine for 24 h, the non-invading cells on the upper surface of each membrane were removed from the chamber by using cotton swabs, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: MicroRNA-375 Functions as a Tumor-Suppressor Gene in Gastric Cancer by Targeting Recepteur d’Origine Nantais
Article Snippet: After 24 h, cells that had invaded the Matrigel and 8-μM pore membrane were fixed and stained with the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Allergen‑removed Rhus verniciflua Stokes suppresses invasion and migration of pancreatic cancer cells through downregulation of the JAK/STAT and Src/FAK signaling pathways.
Article Snippet: The noninvading cells on the upper surface of membrane were removed from the chamber, and the invading cells on the lower surface of the membrane were stained with Quick‐Diff stain kit (BD Biosciences).

Article Title: Inhibition of glioblastoma cell invasion by hsa-miR-145-5p and hsa-miR-31-5p co-overexpression in human mesenchymal stem cells
Article Snippet: The noninvading cells on the upper surface of the membrane of the upper wells were removed, and the invading cells on the lower surface of the membrane were stained with a Quick-Diff stain kit (Becton Dickinson).

Article Title: Cholic Acid Stimulates MMP-9 in Human Colon Cancer Cells via Activation of MAPK, AP-1, and NF-κB Activity
Article Snippet: To determine the effect of signaling inhibitors on CA-induced cell invasion, SW620 cells were preincubated with various ROS scavenger or signaling inhibitors for 1 h and incubated with CA for 24 h. Noninvading cells on the upper surface of each membrane were removed from the chamber, while invading cells on the lower surface of each membrane were stained with a Diff-Quick stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Suppression of Urokinase-Type Plasminogen Activator Receptor by Docosahexaenoic Acid Mediated by Heme Oxygenase-1 in 12- O -Tetradecanoylphorbol-13-Acetate-Induced Human Endothelial Cells
Article Snippet: The non-invading cells on the upper surface of each membrane were removed from the chamber, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, United States).

Staining:

Article Title: Prostaglandin E 2 stimulates urokinase-type plasminogen activator receptor via EP2 receptor-dependent signaling pathways in human AGS gastric cancer cells.
Article Snippet: This article is protected by copyright.. All rights reserved 2 Aberrant expression of urokinase-type plasminogen activator receptor (uPAR) has been observed in human gastric cancers.. Prostaglandin E2 (PGE2), whose biosynthesis is catalyzed by cyclooxygenase-2 (COX-2), is implicated in cancer metastasis; however, the cellular and molecular mechanisms of PGE2-driven uPAR expression are yet to be elucidated in human gastric cancer AGS cells.

Article Title: Docosahexaenoic Acid Inhibits Tumor Promoter-Induced Urokinase-Type Plasminogen Activator Receptor by Suppressing PKCδ- and MAPKs-Mediated Pathways in ECV304 Human Endothelial Cells
Article Snippet: The non-invading cells on the upper surface of each membrane were removed from the chamber by using cotton swabs, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Sulforaphane Suppresses the Nicotine-Induced Expression of the Matrix Metalloproteinase-9 via Inhibiting ROS-Mediated AP-1 and NF-κB Signaling in Human Gastric Cancer Cells
Article Snippet: Briefly, AGS cells were added to the upper chamber with nicotine for 24 h, the non-invading cells on the upper surface of each membrane were removed from the chamber by using cotton swabs, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: MicroRNA-375 Functions as a Tumor-Suppressor Gene in Gastric Cancer by Targeting Recepteur d’Origine Nantais
Article Snippet: After 24 h, cells that had invaded the Matrigel and 8-μM pore membrane were fixed and stained with the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Allergen‑removed Rhus verniciflua Stokes suppresses invasion and migration of pancreatic cancer cells through downregulation of the JAK/STAT and Src/FAK signaling pathways.
Article Snippet: The noninvading cells on the upper surface of membrane were removed from the chamber, and the invading cells on the lower surface of the membrane were stained with Quick‐Diff stain kit (BD Biosciences).

Article Title: Inhibition of glioblastoma cell invasion by hsa-miR-145-5p and hsa-miR-31-5p co-overexpression in human mesenchymal stem cells
Article Snippet: The noninvading cells on the upper surface of the membrane of the upper wells were removed, and the invading cells on the lower surface of the membrane were stained with a Quick-Diff stain kit (Becton Dickinson).

Article Title: Cholic Acid Stimulates MMP-9 in Human Colon Cancer Cells via Activation of MAPK, AP-1, and NF-κB Activity
Article Snippet: To determine the effect of signaling inhibitors on CA-induced cell invasion, SW620 cells were preincubated with various ROS scavenger or signaling inhibitors for 1 h and incubated with CA for 24 h. Noninvading cells on the upper surface of each membrane were removed from the chamber, while invading cells on the lower surface of each membrane were stained with a Diff-Quick stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Suppression of Urokinase-Type Plasminogen Activator Receptor by Docosahexaenoic Acid Mediated by Heme Oxygenase-1 in 12- O -Tetradecanoylphorbol-13-Acetate-Induced Human Endothelial Cells
Article Snippet: The non-invading cells on the upper surface of each membrane were removed from the chamber, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, United States).

Incubation:

Article Title: Prostaglandin E 2 stimulates urokinase-type plasminogen activator receptor via EP2 receptor-dependent signaling pathways in human AGS gastric cancer cells.
Article Snippet: This article is protected by copyright.. All rights reserved 2 Aberrant expression of urokinase-type plasminogen activator receptor (uPAR) has been observed in human gastric cancers.. Prostaglandin E2 (PGE2), whose biosynthesis is catalyzed by cyclooxygenase-2 (COX-2), is implicated in cancer metastasis; however, the cellular and molecular mechanisms of PGE2-driven uPAR expression are yet to be elucidated in human gastric cancer AGS cells.

Article Title: Docosahexaenoic Acid Inhibits Tumor Promoter-Induced Urokinase-Type Plasminogen Activator Receptor by Suppressing PKCδ- and MAPKs-Mediated Pathways in ECV304 Human Endothelial Cells
Article Snippet: The non-invading cells on the upper surface of each membrane were removed from the chamber by using cotton swabs, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Sulforaphane Suppresses the Nicotine-Induced Expression of the Matrix Metalloproteinase-9 via Inhibiting ROS-Mediated AP-1 and NF-κB Signaling in Human Gastric Cancer Cells
Article Snippet: Briefly, AGS cells were added to the upper chamber with nicotine for 24 h, the non-invading cells on the upper surface of each membrane were removed from the chamber by using cotton swabs, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: MicroRNA-375 Functions as a Tumor-Suppressor Gene in Gastric Cancer by Targeting Recepteur d’Origine Nantais
Article Snippet: After 24 h, cells that had invaded the Matrigel and 8-μM pore membrane were fixed and stained with the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Allergen‑removed Rhus verniciflua Stokes suppresses invasion and migration of pancreatic cancer cells through downregulation of the JAK/STAT and Src/FAK signaling pathways.
Article Snippet: The noninvading cells on the upper surface of membrane were removed from the chamber, and the invading cells on the lower surface of the membrane were stained with Quick‐Diff stain kit (BD Biosciences).

Article Title: Inhibition of glioblastoma cell invasion by hsa-miR-145-5p and hsa-miR-31-5p co-overexpression in human mesenchymal stem cells
Article Snippet: The noninvading cells on the upper surface of the membrane of the upper wells were removed, and the invading cells on the lower surface of the membrane were stained with a Quick-Diff stain kit (Becton Dickinson).

Article Title: Cholic Acid Stimulates MMP-9 in Human Colon Cancer Cells via Activation of MAPK, AP-1, and NF-κB Activity
Article Snippet: To determine the effect of signaling inhibitors on CA-induced cell invasion, SW620 cells were preincubated with various ROS scavenger or signaling inhibitors for 1 h and incubated with CA for 24 h. Noninvading cells on the upper surface of each membrane were removed from the chamber, while invading cells on the lower surface of each membrane were stained with a Diff-Quick stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Suppression of Urokinase-Type Plasminogen Activator Receptor by Docosahexaenoic Acid Mediated by Heme Oxygenase-1 in 12- O -Tetradecanoylphorbol-13-Acetate-Induced Human Endothelial Cells
Article Snippet: The non-invading cells on the upper surface of each membrane were removed from the chamber, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, United States).

Diff-Quik:

Article Title: Prostaglandin E 2 stimulates urokinase-type plasminogen activator receptor via EP2 receptor-dependent signaling pathways in human AGS gastric cancer cells.
Article Snippet: This article is protected by copyright.. All rights reserved 2 Aberrant expression of urokinase-type plasminogen activator receptor (uPAR) has been observed in human gastric cancers.. Prostaglandin E2 (PGE2), whose biosynthesis is catalyzed by cyclooxygenase-2 (COX-2), is implicated in cancer metastasis; however, the cellular and molecular mechanisms of PGE2-driven uPAR expression are yet to be elucidated in human gastric cancer AGS cells.

Article Title: Docosahexaenoic Acid Inhibits Tumor Promoter-Induced Urokinase-Type Plasminogen Activator Receptor by Suppressing PKCδ- and MAPKs-Mediated Pathways in ECV304 Human Endothelial Cells
Article Snippet: The non-invading cells on the upper surface of each membrane were removed from the chamber by using cotton swabs, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Sulforaphane Suppresses the Nicotine-Induced Expression of the Matrix Metalloproteinase-9 via Inhibiting ROS-Mediated AP-1 and NF-κB Signaling in Human Gastric Cancer Cells
Article Snippet: Briefly, AGS cells were added to the upper chamber with nicotine for 24 h, the non-invading cells on the upper surface of each membrane were removed from the chamber by using cotton swabs, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: MicroRNA-375 Functions as a Tumor-Suppressor Gene in Gastric Cancer by Targeting Recepteur d’Origine Nantais
Article Snippet: After 24 h, cells that had invaded the Matrigel and 8-μM pore membrane were fixed and stained with the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Allergen‑removed Rhus verniciflua Stokes suppresses invasion and migration of pancreatic cancer cells through downregulation of the JAK/STAT and Src/FAK signaling pathways.
Article Snippet: The noninvading cells on the upper surface of membrane were removed from the chamber, and the invading cells on the lower surface of the membrane were stained with Quick‐Diff stain kit (BD Biosciences).

Article Title: Inhibition of glioblastoma cell invasion by hsa-miR-145-5p and hsa-miR-31-5p co-overexpression in human mesenchymal stem cells
Article Snippet: The noninvading cells on the upper surface of the membrane of the upper wells were removed, and the invading cells on the lower surface of the membrane were stained with a Quick-Diff stain kit (Becton Dickinson).

Article Title: Cholic Acid Stimulates MMP-9 in Human Colon Cancer Cells via Activation of MAPK, AP-1, and NF-κB Activity
Article Snippet: To determine the effect of signaling inhibitors on CA-induced cell invasion, SW620 cells were preincubated with various ROS scavenger or signaling inhibitors for 1 h and incubated with CA for 24 h. Noninvading cells on the upper surface of each membrane were removed from the chamber, while invading cells on the lower surface of each membrane were stained with a Diff-Quick stain kit (Becton-Dickinson, Franklin Lakes, NJ, USA).

Article Title: Suppression of Urokinase-Type Plasminogen Activator Receptor by Docosahexaenoic Acid Mediated by Heme Oxygenase-1 in 12- O -Tetradecanoylphorbol-13-Acetate-Induced Human Endothelial Cells
Article Snippet: The non-invading cells on the upper surface of each membrane were removed from the chamber, and the invading cells on the lower surface of each membrane were stained using the Quick-Diff stain kit (Becton-Dickinson, Franklin Lakes, NJ, United States).



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RBM23 knockdown inhibits colon cancer cell growth and survival (A) Protein was extracted from the normal colon cell lines CCD-18Co and colon cancer cell lines (HCT116, HT29, LOVO, LS513, DLD-1, COLO205, HCT15) and quantified in equal amounts, and then the protein expression of RBM23 was detected by western blotting. (B) The mRNA expression level of RBM23 was measured by qRT-PCR in the normal colon cell line CCD-18Co and colon cancer cell lines (DLD-1, HCT15, HT29, HCT116). GAPDH was used as an internal control for normalization. (C) Western blot analysis was performed to measure the expression levels of c-Myc in HCT15 cells treated with control siRNA or RBM23 siRNA for 72 h. (D) HCT116 cells were treated with control siRNA or RBM23 siRNA #1, #2, #3 for 72 h. Protein expression levels of various factors were then analyzed by western blotting. (E) The effect of RBM23 deficiency on HCT116, a colon cancer cell line. HCT116 was transfected with 80 nM RBM23 siRNA and control siRNA, and cell viability was examined at 0 and 72 h of treatment. Cell viability was measured by CCK8 assay and optical density was measured by microplate reader at 450 nm. Data were normalized to the control siRNA group at 0 h (set as 100%). (F) The effect of RBM23 knockdown in colon cancer cells, HCT116, on cell proliferation. HCT116 cells were transfected with RBM23 siRNA (100 nM) and incubated for one week, and colonies were stained with <t>Diff</t> <t>Quick</t> solution. The colonies were counted and quantified. (G) Western blotting was performed to detect proteins extracted from HCT116 cells fractionated into nucleus and cytoplasm. Proteins from HCT116 cells transfected with RBM23 siRNA (100 nM) for 72 h were extracted and separated by NE-PER nuclear and cytoplasmic extraction kit into proteins extracted from the nucleus and cytoplasm. The proteins were then detected using western blotting. Student’s t -test: ***P < 0.001
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RBM23 knockdown inhibits colon cancer cell growth and survival (A) Protein was extracted from the normal colon cell lines CCD-18Co and colon cancer cell lines (HCT116, HT29, LOVO, LS513, DLD-1, COLO205, HCT15) and quantified in equal amounts, and then the protein expression of RBM23 was detected by western blotting. (B) The mRNA expression level of RBM23 was measured by qRT-PCR in the normal colon cell line CCD-18Co and colon cancer cell lines (DLD-1, HCT15, HT29, HCT116). GAPDH was used as an internal control for normalization. (C) Western blot analysis was performed to measure the expression levels of c-Myc in HCT15 cells treated with control siRNA or RBM23 siRNA for 72 h. (D) HCT116 cells were treated with control siRNA or RBM23 siRNA #1, #2, #3 for 72 h. Protein expression levels of various factors were then analyzed by western blotting. (E) The effect of RBM23 deficiency on HCT116, a colon cancer cell line. HCT116 was transfected with 80 nM RBM23 siRNA and control siRNA, and cell viability was examined at 0 and 72 h of treatment. Cell viability was measured by CCK8 assay and optical density was measured by microplate reader at 450 nm. Data were normalized to the control siRNA group at 0 h (set as 100%). (F) The effect of RBM23 knockdown in colon cancer cells, HCT116, on cell proliferation. HCT116 cells were transfected with RBM23 siRNA (100 nM) and incubated for one week, and colonies were stained with <t>Diff</t> <t>Quick</t> solution. The colonies were counted and quantified. (G) Western blotting was performed to detect proteins extracted from HCT116 cells fractionated into nucleus and cytoplasm. Proteins from HCT116 cells transfected with RBM23 siRNA (100 nM) for 72 h were extracted and separated by NE-PER nuclear and cytoplasmic extraction kit into proteins extracted from the nucleus and cytoplasm. The proteins were then detected using western blotting. Student’s t -test: ***P < 0.001
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RBM23 knockdown inhibits colon cancer cell growth and survival (A) Protein was extracted from the normal colon cell lines CCD-18Co and colon cancer cell lines (HCT116, HT29, LOVO, LS513, DLD-1, COLO205, HCT15) and quantified in equal amounts, and then the protein expression of RBM23 was detected by western blotting. (B) The mRNA expression level of RBM23 was measured by qRT-PCR in the normal colon cell line CCD-18Co and colon cancer cell lines (DLD-1, HCT15, HT29, HCT116). GAPDH was used as an internal control for normalization. (C) Western blot analysis was performed to measure the expression levels of c-Myc in HCT15 cells treated with control siRNA or RBM23 siRNA for 72 h. (D) HCT116 cells were treated with control siRNA or RBM23 siRNA #1, #2, #3 for 72 h. Protein expression levels of various factors were then analyzed by western blotting. (E) The effect of RBM23 deficiency on HCT116, a colon cancer cell line. HCT116 was transfected with 80 nM RBM23 siRNA and control siRNA, and cell viability was examined at 0 and 72 h of treatment. Cell viability was measured by CCK8 assay and optical density was measured by microplate reader at 450 nm. Data were normalized to the control siRNA group at 0 h (set as 100%). (F) The effect of RBM23 knockdown in colon cancer cells, HCT116, on cell proliferation. HCT116 cells were transfected with RBM23 siRNA (100 nM) and incubated for one week, and colonies were stained with <t>Diff</t> <t>Quick</t> solution. The colonies were counted and quantified. (G) Western blotting was performed to detect proteins extracted from HCT116 cells fractionated into nucleus and cytoplasm. Proteins from HCT116 cells transfected with RBM23 siRNA (100 nM) for 72 h were extracted and separated by NE-PER nuclear and cytoplasmic extraction kit into proteins extracted from the nucleus and cytoplasm. The proteins were then detected using western blotting. Student’s t -test: ***P < 0.001
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Image Search Results


RBM23 knockdown inhibits colon cancer cell growth and survival (A) Protein was extracted from the normal colon cell lines CCD-18Co and colon cancer cell lines (HCT116, HT29, LOVO, LS513, DLD-1, COLO205, HCT15) and quantified in equal amounts, and then the protein expression of RBM23 was detected by western blotting. (B) The mRNA expression level of RBM23 was measured by qRT-PCR in the normal colon cell line CCD-18Co and colon cancer cell lines (DLD-1, HCT15, HT29, HCT116). GAPDH was used as an internal control for normalization. (C) Western blot analysis was performed to measure the expression levels of c-Myc in HCT15 cells treated with control siRNA or RBM23 siRNA for 72 h. (D) HCT116 cells were treated with control siRNA or RBM23 siRNA #1, #2, #3 for 72 h. Protein expression levels of various factors were then analyzed by western blotting. (E) The effect of RBM23 deficiency on HCT116, a colon cancer cell line. HCT116 was transfected with 80 nM RBM23 siRNA and control siRNA, and cell viability was examined at 0 and 72 h of treatment. Cell viability was measured by CCK8 assay and optical density was measured by microplate reader at 450 nm. Data were normalized to the control siRNA group at 0 h (set as 100%). (F) The effect of RBM23 knockdown in colon cancer cells, HCT116, on cell proliferation. HCT116 cells were transfected with RBM23 siRNA (100 nM) and incubated for one week, and colonies were stained with Diff Quick solution. The colonies were counted and quantified. (G) Western blotting was performed to detect proteins extracted from HCT116 cells fractionated into nucleus and cytoplasm. Proteins from HCT116 cells transfected with RBM23 siRNA (100 nM) for 72 h were extracted and separated by NE-PER nuclear and cytoplasmic extraction kit into proteins extracted from the nucleus and cytoplasm. The proteins were then detected using western blotting. Student’s t -test: ***P < 0.001

Journal: Cancer Cell International

Article Title: Inhibition of RBM23 induces ferroptosis in colon cancer cells via c-Myc regulation

doi: 10.1186/s12935-026-04262-x

Figure Lengend Snippet: RBM23 knockdown inhibits colon cancer cell growth and survival (A) Protein was extracted from the normal colon cell lines CCD-18Co and colon cancer cell lines (HCT116, HT29, LOVO, LS513, DLD-1, COLO205, HCT15) and quantified in equal amounts, and then the protein expression of RBM23 was detected by western blotting. (B) The mRNA expression level of RBM23 was measured by qRT-PCR in the normal colon cell line CCD-18Co and colon cancer cell lines (DLD-1, HCT15, HT29, HCT116). GAPDH was used as an internal control for normalization. (C) Western blot analysis was performed to measure the expression levels of c-Myc in HCT15 cells treated with control siRNA or RBM23 siRNA for 72 h. (D) HCT116 cells were treated with control siRNA or RBM23 siRNA #1, #2, #3 for 72 h. Protein expression levels of various factors were then analyzed by western blotting. (E) The effect of RBM23 deficiency on HCT116, a colon cancer cell line. HCT116 was transfected with 80 nM RBM23 siRNA and control siRNA, and cell viability was examined at 0 and 72 h of treatment. Cell viability was measured by CCK8 assay and optical density was measured by microplate reader at 450 nm. Data were normalized to the control siRNA group at 0 h (set as 100%). (F) The effect of RBM23 knockdown in colon cancer cells, HCT116, on cell proliferation. HCT116 cells were transfected with RBM23 siRNA (100 nM) and incubated for one week, and colonies were stained with Diff Quick solution. The colonies were counted and quantified. (G) Western blotting was performed to detect proteins extracted from HCT116 cells fractionated into nucleus and cytoplasm. Proteins from HCT116 cells transfected with RBM23 siRNA (100 nM) for 72 h were extracted and separated by NE-PER nuclear and cytoplasmic extraction kit into proteins extracted from the nucleus and cytoplasm. The proteins were then detected using western blotting. Student’s t -test: ***P < 0.001

Article Snippet: The plates were then incubated at 37 °C, 5% CO 2 for 1 week and the colonies were fixed and stained using Diff-Quick Kit (Sysmex Corporation, Kobe, Hyogo, Japan) and the number of colonies was counted.

Techniques: Knockdown, Expressing, Western Blot, Quantitative RT-PCR, Control, Transfection, CCK-8 Assay, Incubation, Staining, Diff-Quik, Extraction