The comparative tests of nine agents were performed twice on different days. heatmap of gene copy number data of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Red color for amplifications, green color for deletions and black color for normal gene copy figures were used. ncomms14098-s5.xlsx (63K) GUID:?7C95C46F-2415-4A1D-936E-2DB6BB4EB912 Supplementary Data 5 A heatmap of RNA content (RNA sequencing) of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Signals are represented as log2(transmission). Green (low) to reddish (high) color level was used. ncomms14098-s6.xlsx (145K) GUID:?59A3AA79-725E-4BAD-B9FD-DBDE0894C5A6 Supplementary Data 6 A heatmap of RNA content (Illumina HumanWG BeadChip microarray analysis) of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Signals are represented as log2(transmission). Green (low) to reddish (high) color level was used. ncomms14098-s7.xlsx (142K) GUID:?55D34330-2E88-40E6-B351-4184AA9BACFA Supplementary Data 7 A heatmap of RNA content (RNA sequencing) of cell lines for the whole genome. Signals are represented as log2(transmission). White (low) to black (high) color level was used. ncomms14098-s8.xlsx (12M) GUID:?B8092680-7620-4D55-B029-054A7F267211 Data Availability StatementPrimary data for this work are contained in Supplementary Data or at GEO as “type”:”entrez-geo”,”attrs”:”text”:”GSE32036″,”term_id”:”32036″GSE32036. Abstract Mutations in the gene resulting in complete loss of its protein (BRG1) occur frequently in non-small cell lung malignancy (NSCLC) cells. Currently, no single therapeutic agent has been identified as synthetically lethal with SMARCA4/BRG1 loss. We identify AURKA activity as essential in NSCLC cells lacking SMARCA4/BRG1. In these cells, RNAi-mediated depletion or chemical inhibition of AURKA induces apoptosis and cell death and in xenograft mouse models. Disc large homologue-associated protein 5 (HURP/DLGAP5), required for AURKA-dependent, centrosome-independent mitotic spindle assembly is essential for the survival and proliferation of mutant but not of SMARCA4/BRG1wild-type cells. AURKA inhibitors may provide a therapeutic strategy for biomarker-driven clinical studies to treat the NSCLCs harbouring in NSCLC cells, we conducted a whole-genome siRNA library screen in a cell collection belonging to a panel of NSCLC-derived cell lines that has been extensively characterized21. From your cell lines harbouring homozygous and Dunnett’s multiple comparison assessments. siRNA transfections were performed in triplicate with pools of 50?nM of four separate siRNA duplexes targeting each of 21,124 genes and cell viability was measured after 96?h. We recognized 880 siRNA pools with Dunnett’s multiple comparison tests. (d) The effect of individual siRNAs on NCI-H1819 cells was measured by immunoblotting with monoclonal antibodies to cleaved poly (ADP-ribose) polymerase 1 (PARP), phospho-Histone H3 and -Actin as a loading control 3 days after transfecting the cells with either non-targeting or TPX2-targeting siRNAs. Cleaved PARP indicated an active apoptotic response and phospho-Histone H3 indicated mitotic arrest. Data are representative of duplicate experiments. (e) Five days after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or individual siRNAs #5 and #6 targeting TPX2, cell viability was measured with a CellTiter-Glo assay that measure cellular ATP as a surrogate for cell proliferation or survival. PLK1 was depleted as the positive control. Error bars on graphs are s.d. of means from triplicate biological replicates. TPX2 is required by NSCLC cells with inactivated showed a large increase in Histone H3 phosphorylation (Fig. 2d). This suggested that lack of TPX2 resulted in delayed exit from or cell cycle arrest in mitosis. To expand our observations to a larger panel of NSCLC lines, we tested two of the most efficacious individual siRNAs targeting on an additional two were more harmful in (Fig. 2e). The cells expressing wild-type were not just less sensitive to inhibitors of mitosis, as all of these NSCLC cell lines were similarly sensitive to the depletion of Dunnett’s multiple comparison assessments) in the average doubling occasions between SMARCA4-null and SMARCA4-wild-type NSCLC lines (Supplementary Table 1). SMARCA4 loss sensitizes to depletion or inhibition of AURKA As TPX2 binds and activates AURKA in mitosis, we depleted AURKA protein with four individual siRNAs to identify the most efficient ones for further experiments (Fig. 3a). Among four siRNAs, only one showed complete knockdown of AURKA, whereas two of the four resulted in partial depletion. Only the most efficient siRNA produced >50% reduction in cell growth, indicating that low levels of AURKA support cell viability (Fig. 3b). Because of its higher efficacy, we used siRNA #28 to deplete AURKA in the following experiments. Depleting AURKA in NCI-H1819 cells induced mitotic arrest and apoptosis (Fig. 3c). To understand whether.After washing with PBS, cells were permeabilized with 0.25% Triton-X in PBS for 15?min at room temperature. values). ncomms14098-s4.xlsx (44K) GUID:?25C731B3-9421-4934-AA5D-DD546B0A111A Supplementary Data 4 A heatmap of gene copy number data of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Red color for amplifications, green color for deletions and black color for normal gene copy numbers were used. ncomms14098-s5.xlsx (63K) GUID:?7C95C46F-2415-4A1D-936E-2DB6BB4EB912 Supplementary Data 5 A heatmap of RNA content (RNA sequencing) of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Signals are represented as log2(signal). Green (low) to red (high) color scale was used. ncomms14098-s6.xlsx (145K) GUID:?59A3AA79-725E-4BAD-B9FD-DBDE0894C5A6 Supplementary Data 6 A heatmap of RNA content (Illumina HumanWG BeadChip microarray analysis) of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Signals are represented as log2(signal). Green (low) to red (high) color scale was used. ncomms14098-s7.xlsx (142K) GUID:?55D34330-2E88-40E6-B351-4184AA9BACFA Supplementary Data 7 A heatmap of RNA content (RNA sequencing) of cell lines for the whole genome. Signals are represented as log2(signal). White (low) to black (high) color scale was used. ncomms14098-s8.xlsx (12M) GUID:?B8092680-7620-4D55-B029-054A7F267211 Data Availability StatementPrimary data for this work are contained in Supplementary Data or at GEO as “type”:”entrez-geo”,”attrs”:”text”:”GSE32036″,”term_id”:”32036″GSE32036. Abstract Mutations in the gene resulting in complete loss of its protein (BRG1) occur frequently in non-small cell lung cancer (NSCLC) cells. Currently, no single therapeutic agent has been identified as synthetically lethal with SMARCA4/BRG1 loss. We identify AURKA activity as essential in NSCLC cells lacking SMARCA4/BRG1. In these cells, RNAi-mediated depletion or chemical inhibition of AURKA induces apoptosis and cell death and in xenograft mouse models. Disc large homologue-associated protein 5 (HURP/DLGAP5), required for AURKA-dependent, centrosome-independent mitotic spindle assembly is essential for the survival and proliferation of mutant but not of SMARCA4/BRG1wild-type cells. AURKA inhibitors may provide a therapeutic strategy for biomarker-driven clinical studies to treat the NSCLCs harbouring in NSCLC cells, we conducted a whole-genome siRNA library screen in a cell line belonging to a panel of NSCLC-derived cell lines that has been extensively characterized21. From the cell lines harbouring homozygous and Dunnett’s multiple comparison tests. siRNA transfections were performed in triplicate with pools of 50?nM of four separate siRNA duplexes targeting each of 21,124 genes and cell viability was measured after 96?h. We identified 880 siRNA pools with Dunnett’s multiple comparison tests. (d) The effect of individual siRNAs on NCI-H1819 cells was measured by immunoblotting with monoclonal antibodies to cleaved poly (ADP-ribose) polymerase 1 (PARP), phospho-Histone H3 and -Actin as a loading control 3 days after transfecting the cells with either non-targeting or TPX2-targeting siRNAs. Cleaved PARP indicated an active apoptotic response and phospho-Histone H3 indicated mitotic arrest. Data are representative of duplicate experiments. (e) Five days after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or individual siRNAs #5 and #6 targeting TPX2, cell viability was measured with a CellTiter-Glo assay that measure cellular ATP as a surrogate for cell proliferation or survival. PLK1 was depleted as the positive control. Error bars on graphs are s.d. of means from triplicate biological replicates. TPX2 is required by NSCLC cells with inactivated showed a large increase in Histone H3 phosphorylation (Fig. 2d). This suggested that lack of TPX2 resulted in delayed exit from or cell cycle arrest in mitosis. To expand our observations to a larger panel of NSCLC lines, we tested two of the most efficacious individual siRNAs targeting on an additional two were more toxic in (Fig. 2e). The cells expressing wild-type were not simply less sensitive to inhibitors of mitosis, as all of these NSCLC cell lines were similarly sensitive to the depletion of Dunnett’s multiple comparison tests) in the average doubling times between SMARCA4-null and SMARCA4-wild-type NSCLC lines (Supplementary Table 1). SMARCA4 loss sensitizes to depletion or inhibition of AURKA As TPX2 binds and activates AURKA in mitosis, we depleted AURKA protein with four individual siRNAs to identify the most efficient ones for further experiments (Fig. 3a). Among four siRNAs, only one showed complete knockdown of AURKA, whereas two of the four resulted in partial depletion..helped design and direct the animal studies. 4 A heatmap of gene copy quantity data of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Red color for amplifications, green color for deletions and black color for normal gene copy figures were used. ncomms14098-s5.xlsx (63K) GUID:?7C95C46F-2415-4A1D-936E-2DB6BB4EB912 Supplementary Data 5 A heatmap of RNA content material (RNA sequencing) of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Signals are displayed as log2(transmission). Green (low) to reddish (high) color level was used. ncomms14098-s6.xlsx (145K) GUID:?59A3AA79-725E-4BAD-B9FD-DBDE0894C5A6 Supplementary Data 6 A heatmap of RNA content (Illumina HumanWG BeadChip microarray analysis) of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Signals are displayed as log2(transmission). Green (low) to reddish (high) color level was used. ncomms14098-s7.xlsx (142K) GUID:?55D34330-2E88-40E6-B351-4184AA9BACFA Supplementary Data 7 A heatmap of RNA content (RNA sequencing) of cell lines for the whole genome. Signals are displayed as log2(transmission). White colored (low) to black (high) Mouse monoclonal to HER2. ErbB 2 is a receptor tyrosine kinase of the ErbB 2 family. It is closely related instructure to the epidermal growth factor receptor. ErbB 2 oncoprotein is detectable in a proportion of breast and other adenocarconomas, as well as transitional cell carcinomas. In the case of breast cancer, expression determined by immunohistochemistry has been shown to be associated with poor prognosis. color level was used. ncomms14098-s8.xlsx (12M) GUID:?B8092680-7620-4D55-B029-054A7F267211 Data Availability StatementPrimary data for this work are contained in Supplementary Data or at GEO as “type”:”entrez-geo”,”attrs”:”text”:”GSE32036″,”term_id”:”32036″GSE32036. Abstract Mutations in the gene resulting in complete loss of its protein (BRG1) occur regularly in non-small cell lung malignancy (NSCLC) cells. Currently, no single restorative agent has been identified as synthetically lethal with SMARCA4/BRG1 loss. We determine AURKA activity as essential in NSCLC cells lacking SMARCA4/BRG1. In these cells, RNAi-mediated depletion or chemical inhibition of AURKA induces apoptosis and cell death and in xenograft mouse models. Disc large homologue-associated protein 5 (HURP/DLGAP5), required for AURKA-dependent, centrosome-independent mitotic spindle assembly is essential for the survival and proliferation of mutant but not of SMARCA4/BRG1wild-type cells. AURKA inhibitors may provide a restorative strategy for biomarker-driven medical studies to treat the NSCLCs harbouring in NSCLC cells, we carried out a whole-genome siRNA library screen inside a cell collection belonging to a panel of NSCLC-derived cell lines that has been extensively characterized21. From your cell lines harbouring homozygous and Dunnett’s multiple assessment checks. siRNA transfections were performed in triplicate with swimming pools of 50?nM of four separate siRNA duplexes targeting each of 21,124 genes and cell viability was measured after 96?h. We recognized 880 siRNA swimming pools with Dunnett’s multiple assessment tests. (d) The effect of individual siRNAs on NCI-H1819 cells was measured by immunoblotting with monoclonal antibodies to cleaved poly (ADP-ribose) polymerase 1 (PARP), phospho-Histone H3 and -Actin like a loading control 3 days after transfecting the cells with either non-targeting or TPX2-focusing on siRNAs. Cleaved PARP indicated an Azathramycin active apoptotic response and phospho-Histone H3 indicated mitotic arrest. Data are representative of duplicate experiments. (e) Five days after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or individual siRNAs #5 and #6 focusing on TPX2, cell viability was measured having a CellTiter-Glo assay that measure cellular ATP like a surrogate for cell proliferation or survival. PLK1 was depleted as the positive control. Error bars on graphs are s.d. of means from triplicate biological replicates. TPX2 is required by NSCLC cells with inactivated showed a large increase in Histone H3 phosphorylation (Fig. 2d). This suggested that lack of TPX2 resulted in delayed exit from or cell cycle arrest in mitosis. To increase our observations to a larger panel of NSCLC lines, we tested two of the most efficacious individual siRNAs focusing on on an additional two were more harmful in (Fig. 2e). The cells expressing wild-type were not simply less sensitive to inhibitors of mitosis, as all of these NSCLC.Both SMARCA2 and EZH2 siRNAs were toxic in our primary screen, but with inside a SMARCA4-null background inhibits cell growth over a period longer than the 96?h of our siRNA assay, probably explaining so why a partial effect was seen. for deletions and black color for normal gene copy figures were used. ncomms14098-s5.xlsx (63K) GUID:?7C95C46F-2415-4A1D-936E-2DB6BB4EB912 Supplementary Data 5 A heatmap of RNA content material (RNA sequencing) of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Signals are displayed as log2(transmission). Green (low) to reddish (high) color level was used. ncomms14098-s6.xlsx (145K) GUID:?59A3AA79-725E-4BAD-B9FD-DBDE0894C5A6 Supplementary Data 6 A heatmap of RNA content (Illumina HumanWG BeadChip microarray analysis) of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Signals are displayed as log2(transmission). Green (low) to reddish (high) color level was used. ncomms14098-s7.xlsx (142K) GUID:?55D34330-2E88-40E6-B351-4184AA9BACFA Supplementary Data 7 A heatmap of RNA content (RNA sequencing) of cell lines for the whole genome. Signals are displayed as log2(transmission). White colored (low) to black (high) color level was used. ncomms14098-s8.xlsx (12M) GUID:?B8092680-7620-4D55-B029-054A7F267211 Data Availability StatementPrimary data for this work are contained in Supplementary Data or at GEO as “type”:”entrez-geo”,”attrs”:”text”:”GSE32036″,”term_id”:”32036″GSE32036. Abstract Mutations in the gene resulting in complete loss of its protein (BRG1) occur regularly in non-small cell lung malignancy (NSCLC) cells. Currently, no single restorative agent continues to be defined as synthetically lethal with SMARCA4/BRG1 reduction. We recognize AURKA activity as important in NSCLC cells missing SMARCA4/BRG1. In these cells, RNAi-mediated depletion or chemical substance inhibition of AURKA induces apoptosis and cell loss of life and in xenograft mouse versions. Disc huge homologue-associated proteins 5 (HURP/DLGAP5), necessary for AURKA-dependent, centrosome-independent mitotic spindle set up is vital for the success and proliferation of mutant however, not of SMARCA4/BRG1wild-type cells. AURKA inhibitors might provide a healing technique for biomarker-driven scientific studies to take care of the NSCLCs harbouring in NSCLC cells, we executed a whole-genome siRNA collection screen within a cell series owned by a -panel of NSCLC-derived cell lines that is extensively characterized21. In the cell lines harbouring homozygous and Dunnett’s multiple evaluation lab tests. siRNA transfections had been performed in triplicate with private pools of 50?nM of four individual siRNA duplexes targeting each of 21,124 genes and cell viability was measured after 96?h. We discovered 880 siRNA private pools with Dunnett’s multiple evaluation tests. (d) The result of specific siRNAs on NCI-H1819 cells was assessed by immunoblotting with monoclonal antibodies to cleaved poly (ADP-ribose) polymerase 1 (PARP), phospho-Histone H3 and -Actin being a launching control 3 times after transfecting the cells with either non-targeting or TPX2-concentrating on siRNAs. Cleaved PARP indicated a dynamic apoptotic response and phospho-Histone H3 indicated mitotic arrest. Data are representative of duplicate tests. (e) Five times after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or specific siRNAs #5 and #6 concentrating on TPX2, cell viability was assessed using a CellTiter-Glo assay that measure mobile ATP being a surrogate for cell proliferation or success. PLK1 was depleted as the positive control. Mistake pubs on graphs are s.d. of means from triplicate natural replicates. TPX2 is necessary by NSCLC cells with inactivated demonstrated a large upsurge in Histone H3 phosphorylation (Fig. 2d). This recommended that insufficient TPX2 led to delayed leave from or cell routine arrest in mitosis. To broaden our observations to a more substantial -panel of NSCLC lines, we examined two of the very most efficacious specific siRNAs concentrating on on yet another two had been more dangerous in (Fig. 2e). The cells expressing wild-type weren’t simply less delicate to inhibitors of mitosis, as many of these NSCLC cell lines had been similarly sensitive towards the depletion of Dunnett’s multiple evaluation lab tests) in the common doubling situations between SMARCA4-null and SMARCA4-wild-type NSCLC lines (Supplementary Desk 1). SMARCA4 reduction sensitizes to depletion or inhibition of AURKA As TPX2 binds and activates AURKA in mitosis, we depleted AURKA proteins with four specific siRNAs to recognize the most effective ones for even more tests (Fig. 3a). Among four siRNAs, only 1 showed comprehensive knockdown of AURKA, whereas two from the four led to partial depletion. Just the most effective siRNA created >50% decrease in cell development, indicating that low degrees of AURKA support cell viability (Fig. 3b). Due to its higher efficiency, we utilized siRNA #28 to deplete AURKA in the.and A.F.G. cell series name, COSMIC Identification for SMARCA4 mutation position (if is available), tissues type, cancers type and medication awareness data (mean of EC50 beliefs). ncomms14098-s4.xlsx (44K) GUID:?25C731B3-9421-4934-AA5D-DD546B0A111A Supplementary Data 4 A heatmap of gene copy number data of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Red colorization for amplifications, green color for deletions and dark color for regular gene copy quantities had been utilized. ncomms14098-s5.xlsx (63K) GUID:?7C95C46F-2415-4A1D-936E-2DB6BB4EB912 Supplementary Data 5 A heatmap of RNA articles (RNA sequencing) of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Indicators are symbolized as log2(indication). Green (low) to crimson (high) color range was utilized. ncomms14098-s6.xlsx (145K) GUID:?59A3AA79-725E-4BAD-B9FD-DBDE0894C5A6 Supplementary Data 6 A heatmap of RNA content (Illumina HumanWG BeadChip microarray analysis) of cell lines for SMARCA4, AURKA, HURP, TPX2, RAN and MYC. Indicators are symbolized as log2(indication). Green (low) to reddish colored (high) color size was utilized. ncomms14098-s7.xlsx (142K) GUID:?55D34330-2E88-40E6-B351-4184AA9BACFA Supplementary Data 7 A heatmap of RNA content material (RNA sequencing) of cell lines for your genome. Indicators are symbolized as log2(sign). Light (low) to dark (high) color size was utilized. ncomms14098-s8.xlsx (12M) GUID:?B8092680-7620-4D55-B029-054A7F267211 Data Availability StatementPrimary data because of this work are within Supplementary Data or at GEO as “type”:”entrez-geo”,”attrs”:”text”:”GSE32036″,”term_id”:”32036″GSE32036. Abstract Mutations in the gene leading to complete lack of its proteins (BRG1) occur often in non-small cell lung tumor (NSCLC) cells. Presently, no healing agent continues to be defined as synthetically lethal with SMARCA4/BRG1 reduction. We recognize AURKA activity as important in NSCLC cells missing SMARCA4/BRG1. In these cells, RNAi-mediated depletion or chemical substance inhibition of AURKA induces apoptosis and cell loss of life and in xenograft mouse versions. Disc huge homologue-associated proteins 5 (HURP/DLGAP5), necessary for AURKA-dependent, centrosome-independent mitotic spindle set up is vital for the success and proliferation of mutant however, not of SMARCA4/BRG1wild-type cells. AURKA inhibitors might provide a healing technique for biomarker-driven scientific studies to take care of the NSCLCs harbouring in NSCLC cells, we executed a whole-genome siRNA collection screen within a cell range owned by a -panel of NSCLC-derived cell lines that is extensively characterized21. Through the cell lines harbouring homozygous and Dunnett’s multiple evaluation exams. siRNA transfections had been performed in triplicate with private pools of 50?nM of four individual siRNA duplexes targeting each of 21,124 genes and cell viability was measured after 96?h. We determined 880 siRNA private pools with Dunnett’s multiple evaluation tests. (d) The result Azathramycin of specific siRNAs on NCI-H1819 cells was assessed by immunoblotting with monoclonal antibodies to cleaved poly (ADP-ribose) polymerase 1 (PARP), phospho-Histone H3 and -Actin being a launching control 3 times after transfecting the cells with either non-targeting or TPX2-concentrating on siRNAs. Cleaved PARP indicated a dynamic apoptotic response and phospho-Histone H3 indicated mitotic arrest. Data are representative of duplicate tests. (e) Five times after transfecting NCI-H1819, NCI-1299, NCI-H23, HCC827 and Calu-1 cells with non-targeting or specific siRNAs #5 and #6 concentrating on TPX2, cell viability was assessed using a CellTiter-Glo assay that measure mobile ATP being a surrogate for cell proliferation or success. PLK1 was depleted as the positive control. Mistake pubs on graphs are s.d. of means from triplicate natural replicates. TPX2 Azathramycin is necessary by NSCLC cells with inactivated demonstrated a large upsurge in Histone H3 phosphorylation (Fig. 2d). This recommended that insufficient TPX2 led to delayed leave from or cell routine arrest in mitosis. To broaden our observations to a more substantial -panel of NSCLC lines, we examined two of the very most efficacious specific siRNAs concentrating on on yet another two had been more poisonous in (Fig. 2e). The cells expressing wild-type weren’t simply less delicate to inhibitors of mitosis, as many of these NSCLC cell lines had been similarly sensitive towards the depletion of Dunnett’s multiple evaluation exams) in the common doubling moments between SMARCA4-null and SMARCA4-wild-type NSCLC lines (Supplementary Desk 1). SMARCA4 reduction sensitizes to depletion or inhibition of AURKA As TPX2 binds and activates AURKA in mitosis, we depleted AURKA proteins with four specific siRNAs to recognize the most effective ones for even more tests (Fig. 3a). Among four siRNAs, only 1 showed full knockdown of AURKA, whereas two from the four led to partial depletion. Just the most effective siRNA created >50% decrease in cell development, indicating that low degrees of AURKA support cell viability (Fig. 3b). Due to its higher efficiency, we utilized siRNA #28 to deplete AURKA in the next tests. Depleting AURKA in NCI-H1819 cells induced mitotic arrest and apoptosis (Fig. 3c). To comprehend whether awareness to AURKA depletion is certainly associated with SMARCA4 Azathramycin reduction causatively, we restored wild-type appearance in the NCI-H1819 cell range (Fig. 1b) and performed similar cell toxicity assays with both parental and SMARCA4-expressing NCI-H1819 cells. Appearance of exogenous SMARCA4 reduced the response to AURKA knockdown significantly.