Browse
Submit Data
Databases
API
Help

Dataset Information

22 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromodomain-helicase-DNA-binding protein 1-like (CHD1L) silencing inhibits gastric cancer cell proliferation, invasion, and migration

ABSTRACT:

Background

We aimed to investigate the effect of chromodomain-helicase-DNA-binding protein 1-like (CHD1L) silencing on the biological behavior of gastric cancer cells.

Methods

Small hairpin RNA (shRNAs) targeting CHD1L were designed and transduced into BGC-823 human gastric cancer cells. Expression of p53, p21, nerve growth factor IB (Nur77), and ARHGEF9 was assessed by western blotting, and the effect of CHD1L silencing on gastric cancer cell proliferation, apoptosis, and migration was examined by MTT, flow cytometry, and wound healing assays, respectively.

Results

In CHD1L-shRNA-1-treated cells, the expression of p53, p21, Nur77, and ARHGEF9 was significantly upregulated, and the number of apoptotic cells was significantly increased compared to the shRNA-negative control (NC; P<0.05). Additionally, the number of cells in the G1 phase was significantly increased among CHD1L-shRNA-1-treated cells. In contrast, the number of cells in the S phase was significantly decreased among CHD1L-shRNA-1-treated cells compared to shRNA-NC-treated cells (P<0.05). Following CHD1L silencing, there were 58.63±10.97 invading cells compared to 144.95±12.68 and 148.49±17.86 in the shRNA-NC and untreated groups, respectively (P<0.05). After 24 h, CHD1L-silenced BGC-823 cells migrated 0.54±0.34 µm compared to 1.34±0.26 and 1.31±0.31 µm in the shRNA-NC and untreated groups, respectively (P<0.05).

Conclusions

CHD1L silencing significantly inhibited the proliferation, invasion, and migration of BGC-823 gastric cancer cells and induced apoptosis. Knockdown of CHD1L may present a novel approach for treating gastric cancer.

SUBMITTER: Li D

PROVIDER: S-EPMC8798113 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

MiR‑500a‑5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5.

Project description:Glioblastoma is one of the most common malignant primary tumors and develops in brain. The molecular mechanism that regulates glioblastoma occurrence still remains unknown. MicroRNA (miR)‑500a‑5p has been reported to be involved in hepatocellular carcinoma and breast cancer. Whether miR‑500a‑5p regulates glioblastoma progression requires further investigation. In the present study, miR‑500a‑5p was highly expressed in malignant glioblastoma tissues and cell lines. Overexpression of miR‑500a‑5p promoted glioblastoma cell proliferation, migration and invasion in vitro. In addition, knockdown of miR‑500a‑5p accelerated cell apoptosis. Furthermore, miR‑500a‑5p inhibition significantly impaired tumor growth in vivo. The present study further explored the downstream mechanism. The luciferase reporter assay revealed that miR‑500a‑5p directly binds the 3'‑untranslated region of chromodomain helicase DNA binding protein 5 (CHD5) mRNA. MiR‑500a‑5p markedly inhibited CHD5 expression in glioblastoma cells. Furthermore, CHD5 was downregulated in glioblastoma tissues, and the expression levels of miR‑500a‑5p and CHD5 were inversely correlated. In addition, knockdown of CHD5 restored the inhibition of cell proliferation and migration triggered by miR‑500a‑5p silence. Finally, it was demonstrated that miR‑500a‑5p can serve as a novel biomarker for the diagnosis and prognosis of glioblastoma patients. Taken together, the results of the present study indicated that miR‑500a‑5p may have promoted glioblastoma development and progression by targeting CHD5.

| S-EPMC6102694 | biostudies-literature

Chromodomain Helicase/ATPase DNA-Binding Protein 1-Like Gene (CHD1L) Expression and Implications for Invasion and Metastasis of Breast Cancer.

Project description:BackgroundChromodomain helicase/ATPase DNA-binding protein 1-like gene (CHD1L), also known as ALC1 (amplified in liver cancer 1 gene), is a new oncogene amplified in many solid tumors. Whether this gene plays a role in invasion and metastasis of breast cancer is unknown.MethodsImmunohistochemistry was performed to detect the expression of CHD1L in patients with invasive ductal carcinoma and normal mammary glands. Chemotaxis, wound healing, and Transwell invasion assays were also performed to examine cell migration and invasion. Western blot analysis was conducted to detect the expression of CHD1L, MMP-2, MMP-9, pAkt/Akt, pARK5/ARK5, and pmTOR/mTOR. Moreover, ELISA was carried out to detect the expression levels of MMP-2 and MMP-9. Nude mice xenograft model was used to detect the invasion and metastasis of breast cancer cell lines.ResultsCHD1L overexpression was observed in 112 of 268 patients (41.8%). This overexpression was associated with lymph node metastasis (P = 0.008), tumor differentiation (P = 0.020), distant metastasis (P = 0.026), MMP-2 (P = 0.035), and MMP-9 expression (P = 0.022). In the cell experiment, reduction of CHD1L inhibited the invasion and metastasis of breast cancer cells by mediating MMP-2 and MMP-9 expression. CHD1L knockdown via siRNA suppressed EGF-induced pAkt, pARK5, and pmTOR. This knockdown inhibited the metastasis of breast cancer cells into the lungs of SCID mice.ConclusionsCHD1L promoted the invasion and metastasis of breast cancer cells via the PI3K/Akt/ARK5/mTOR/MMP signaling pathway. This study identified CHD1L as a potential anti-metastasis target for therapeutic intervention in breast cancer.

| S-EPMC4657932 | biostudies-literature

Silencing the double-stranded RNA binding protein DGCR8 inhibits ovarian cancer cell proliferation, migration, and invasion.

Project description:To evaluate the role of DiGeorge Critical Region 8 (DGCR8), a key component of miRNA biogenesis pathway in ovarian cancer.The expression of DGCR8 in ovarian cancer was detected by immunostaining and DGCR8 knockdown in ovarian cancer cells was achieved using lentiviral shRNA. Differential expression of miRNAs was determined using Nanostring miRNA arrays and validated by real-time RT-PCR.DGCR8 was highly expressed in ovarian cancer. Knockdown of DGCR8 expression inhibits cell proliferation, migration, and invasion, as well as sensitizes cells to apoptosis induced by the chemotherapeutic drug cisplatin. Cellular survival pathways including ERK1/2 mitogen-activated protein kinase and phosphatidylinositol 3-kinase/AKT were attenuated in DGCR8 knockdown cells. DGCR8 knockdown results in dysregulated miRNA gene expression. miR-27b was identified as the most highly down-regulated miRNA in DGCR8 knockdown cells and promoted cell proliferation in ovarian cancer cells.DGCR8 functions as an oncogene in ovarian cancer, which is in part mediated by miR-27b.

| S-EPMC3984613 | biostudies-literature

PLCD3 inhibits apoptosis and promotes proliferation, invasion and migration in gastric cancer.

Project description:Gastric cancer (GC) is a heterogeneous disease whose development is accompanied by alterations in a variety of pathogenic genes. The phospholipase C Delta 3 enzyme is a member of the phospholipase C family, which controls substance transport between cells in the body. However, its role in gastric cancer has not been discovered. The purpose of this study was to investigate the expression and mechanism of action of PLCD3 in connection to gastric cancer. By Western blot analysis and immunohistochemistry, PLCD3 mRNA and protein expression levels were measured, with high PLCD3 expression suggesting poor prognosis. In N87 and HGC-27 cells, the silencing of PLCD3 using small interfering RNA effectively induced apoptosis and inhibited tumor cell proliferation, invasion, and migration. Conversely, overexpression of PLCD3 using overexpressed plasmids inhibited apoptosis in AGS and BGC-823 cells and promoted proliferation, migration, and invasion. In order to investigate the underlying mechanisms, we conducted further analysis of PLCD3, which indicates that this protein is closely related to the cell cycle and EMT. Additionally, we found that overexpression of PLCD3 inhibits apoptosis and promotes the development of GC cells through JAK2/STAT3 signaling. In conclusion, PLCD3 inhibits apoptosis and promotes proliferation, invasion, and migration, which indicated that PLCD3 might serve as a therapeutic target for gastric cancer.

| S-EPMC10837395 | biostudies-literature

Demethylzeylasteral inhibits proliferation, migration, and invasion through FBXW7/c-Myc axis in gastric cancer.

Project description:Gastric cancer (GC) is one of the most familiar malignancy in the digestive system. Demethylzeylasteral (Dem), a natural functional monomer extracted from Tripterygium wilfordii Hook F, shows anti-tumor effects in a variety of cancers, including GC, however, with the underlying mechanism poorly understood. In our study, we show that Dem inhibits the proliferation, migration, and invasion of GC cells, which are mediated by down-regulating c-Myc protein levels. Mechanistically, Dem reduces the stability of c-Myc by up-regulating FBXW7, an E3 ubiquitin ligase. Moreover, in xenograft tumor model experiment, Dem also inhibits GC, which depends on suppressing c-Myc expression. Finally, Dem enhances GC cell chemosensitivity to the combination treatment of 5-Fluorouracil (5-Fu) and doxorubicin (DOX) in vitro. Together, Dem exerts anti-neoplastic activities through destabilizing and suppressing c-Myc, establishing a theory foundation for using it in future treatment of GC.

| S-EPMC8554662 | biostudies-literature

MicroRNA-103a inhibits gastric cancer cell proliferation, migration and invasion by targeting c-Myb.

Project description:ObjectivesThere have been no previous reports concerning functions of miR-103a in gastric cancer (GC) cells. Thus the aim of the study was to investigate its expression and role in development of this tumour.Materials and methodsReal-time RT-PCR was performed to detect expression of miR-103a in GC cell lines and clinical cancer specimens. To further understand its role, we restored expression of miR-103a in MGC-803 cell line by transfection with miR-103a mimics or inhibitors. Effects of miR-103a on cell proliferation, migration and invasion on targets were also determined.ResultsmiR-103a was down-regulated in both GC cell lines and clinical cancer specimens. Meanwhile, its level was closely associated with pM or pTNM stage of GC. Overexpression of miR-103a markedly suppressed proliferation, migration, and invasion of GC cells, while its inhibition significantly accelerated cell proliferation, migration and invasion. Moreover, c-Myb was identified to be a functional downstream target of miR-103a, ectopic expression of which partially reversed suppression of cell proliferation and invasion.ConclusionsThus our observations suggest that miR-103a functioned as a tumour suppressor by targeting c-Myb. These findings indicate that miR-103a might play a significant role in pathogenesis of GC.

| S-EPMC6496034 | biostudies-literature

Overexpression of chromodomain helicase DNA binding protein 5 (CHD5) inhibits cell proliferation and induces cell cycle arrest and apoptosis in chronic myeloid leukemia

Project description:Background Chromodomain helicase DNA binding protein 5 (CHD5) was reported to be a tumor suppressor and our previous work showed CHD5 was epigenetically inactivated in human chronic myeloid leukemia (CML). This study aimed to investigate the effect of its overexpression on CML tumorigenesis. Methods Quantitative reverse-transcriptase PCR and Western blotting analysis were used to detect the expression of CHD5 in human CML cell lines. The endogenous CHD5 expression was activated in two CML cell lines by CRISPR/dCas9-SAM system. In vitro cell function experiments were performed including proliferation, colony formation, apoptosis, autophagy, senescence and differentiation assays. Furthermore, tumorigenicity was evaluated in vivo in nude mice xenograft model. Results CHD5 was down-regulated in CML cell lines compare to normal bone marrow mononuclear cells (MCs). Cell proliferation after activating CHD5 was significantly inhibited. Moreover, overexpression of CHD5 induced G2/M phase arrest and apoptosis in CML cells. In a tumor xenograft mouse model, CHD5 restoration was found to sharply repress tumor growth. Compared with the control group, overexpression of CHD5 enhanced the expression of p21 and cdc2 phosphorylation, whereas decreased the protein level of Cyclin B1. Furthermore, experiments revealed that up-regulation of CHD5 activated caspase-3, while anti-apoptosis protein Bcl-2 expression was reduced in CML cells. Conclusions CHD5 plays a role of anti-tumorigenic effects involved in CML cell proliferation, cell cycle arrest and apoptosis.

| S-EPMC8797277 | biostudies-literature

Cir-ITCH inhibits gastric cancer migration, invasion and proliferation by regulating the Wnt/β-catenin pathway.

Project description:Circular RNAs (circRNAs) are differentially expressed in various tumours, but the expression and regulatory mechanisms of circular RNA ITCH (cir-ITCH) in gastric cancer remain unclear. For this reason, in the present study, we assessed the expression of cir-ITCH and the associated regulatory mechanism of cir-ITCH in gastric cancer. Through RTq-PCR assays, we observed that cir-ITCH expression was attenuated in gastric cancer cell lines and tissues, with cir-ITCH expression in gastric cancer tissues with lymph node metastasis being considerably lower than that observed in gastric cancer tissues without lymph node metastasis. In addition, we demonstrated that cir-ITCH or linear ITCH may be a useful marker for gastric cancer prognosis by Kaplan-Meier survival analysis. We also showed that cir-ITCH overexpression could increase linear ITCH expression through miR-17 via RNA immunoprecipitation (RIP) and luciferase reporter assays. Moreover, in vivo and in vitro experimental results showed that cir-ITCH can act as a tumour suppressor to prevent gastric cancer tumourgenesis by sponging miR-17. The Wnt/β-catenin pathway plays a crucial role during the carcinogenesis of cancers, and we observed that cir-ITCH could negatively regulate Wnt/β-catenin signalling, which could be restored by miR-17. In summary, cir-ITCH was shown to prevent gastric cancer tumourgenesis through the Wnt/β-catenin signalling pathway by sequestering miR-17.

| S-EPMC7566509 | biostudies-literature

RPS15a Silencing Suppresses Cell Proliferation and Migration of Gastric Cancer.

Project description:PurposeInformation on the possible role of the ribosomal protein S15a (RPS15a) in gastric cancer is scarce. The aim of this study was to evaluate the impact of RPS15a gene expression on the growth and cell cycle of gastric cancer cells in vitro and in vivo.Materials and methodsRPS15a mRNA expression was examined in cancer tissues and their corresponding adjacent normal tissues of 40 gastric adenocarcinoma patients. Next, RPS15a was knocked down using a lentivirus-mediated RNA interference (short hairpin RNA) system in the gastric cancer cell line BGC823. The effect of RPS15a knockdown was examined using CCK-8 assay, cell scratch test, colony formation assay, and flow cytometry. Finally, in nude mice, a tumorigenicity test was performed, and the tumor volume and weight were measured.ResultsRPS15a expression in tumor tissue was significantly greater than that in the adjacent normal tissue of gastric cancer patients. After RPS15a silencing, the BGC823 cell proliferation rate decreased significantly; most cells were arrested in the G0/G1 phase, cell growth was inhibited, and the migration rate was decreased. Colony formation assay showed that the number and size of clones in the RPS15a-silenced cells were fewer and smaller, compared to control cells. The nude mouse tumorigenicity test showed that RPS15a silencing had an inhibitory effect on tumor volume and mice weight.ConclusionThe present study found RPS15a expression to be higher in gastric tumors and its silencing in gastric cancer cells to inhibit the proliferation, growth, and migration thereof. Accordingly, RPS15a may be considered as a potential therapeutic target in gastric cancer.

| S-EPMC6240561 | biostudies-literature

GATA1 gene silencing inhibits invasion, proliferation and migration of cholangiocarcinoma stem cells via disrupting the PI3K/AKT pathway.

Project description:Background/aims: Intrahepatic cholangiocarcinoma (CCA) is the second most prevalent type primary liver malignancy, accompanied by an increasing global incidence and mortality rate. Research has documented the contribution of the GATA binding protein-1 (GATA1) in the progression of liver cancer. Here, we aim to investigate the role of GATA1 in CCA stem cells via the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway. Methods: Initially, microarray-based gene expression profiling was employed to identify the differentially expressed genes associated with CCA. Subsequently, an investigation was conducted to explore the potential biological significance behind the silencing of GATA1 and the regulatory mechanism between GATA1 and PI3K/AKT pathway. CCA cell lines QBC-939 and RBE were selected and treated with siRNA against GATA1 or/and a PI3K/AKT pathway inhibitor LY294002. In vivo experiment was also conducted to confirm in vitro findings. Results: GATA1 exhibited higher expression in CCA samples and was predicted to affect the progression of CCA through blockade of the PI3K/AKT pathway. siRNA-mediated downregulation of GATA1 and LY294002 treatment resulted in reduced proliferation, migration and invasion abilities of CCA stem cells, together with impeded tumor growth, and led to increased cell apoptosis and primary cilium expression. Additionally, the siRNA-mediated GATA1 downregulation had an inhibitory effect on the PI3K/AKT pathway. LY294002 was manifested to enhance the inhibitory effects of GATA1 inhibition on CCA progression. These in vitro findings were reproduced in vivo on siRNA against GATA1 or LY294002 injected nude mice. Conclusion: Altogether, the present study highlighted that downregulation of GATA1 via blockade of the PI3K/AKT pathway could inhibit the CCA stem cell proliferation, migration and invasion, and tumor growth, and promote cell apoptosis, primary cilium expression.

| S-EPMC6620705 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data