Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse liver from p53-/- animals with Ad TRF2DBDM compared to Ad GFP (2x10^10 PFU) (GSM103546, GSM103547) to investigate telomere dysfunction

ABSTRACT: We used microarrays to analyze the prevalence of signalling induced by acute telomere dysfunction (as induced by TRF2DBDM expression = Dataset 1) and in TERC- compared to TERC+ HCC (Dataset 2). Experiment Overall Design: Presented are gene expression data from: Experiment Overall Design: Dataset 1: Mouse liver 48h after i.v. infection of p53-/- mice with Ad TRF2DBDM compared to Ad GFP (2x10^10 PFU) (GSM103546, GSM103547) and Experiment Overall Design: Dataset 2: p53-/- heptaocellular carcinoma (HCC) from mTERC+ HBs (GSM103548, GSM103549, GSM103553) compared to mTERC-, HBs (GSM103550, GSM103551, GSM103552) transgenic mice. Experiment Overall Design: All mice were in a C57BL/6J background. Experiment Overall Design: Dataset 1: Liver RNA was extracted 48h after adenoviral infection (n=3 mice/group), samples were pooled for hybridization on Affymetrix microarrays. Experiment Overall Design: Dataset 2: RNA was extracted from HCC of 12-15month old mTERC+ and mTERC- mice (n=3 mice/group). Individual tumors were hybridized on Affymetrix microarrays. Experiment Overall Design: Differentially expressed gene clusters were identified using Array Assist 4.0 (Stratagene).

ORGANISM(S): Mus musculus

SUBMITTER: Robert Geffers

PROVIDER: E-GEOD-4627 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Background: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide, with unclear pathogenesis. Sphingomyelin phodiesterase acid-like 3A (SMPDL3A) affects cell differentiation and participates in immune regulation. However, its molecular biological function in HCC has not yet been elucidated. Methods：Data from 180 HCC patients were analyzed the relationship between the expression of SMPDL3A in liver cancer tissues and the prognosis of liver cancer patients. Crispr-Cas9 dual vector lentivirus was used to knock out SMPDL3A in HCC cell lines. The effects of SMPDL3A on cell viability were determined by CCK8 assay, clone formation experiment, cell cycle assay, cell scratch, TUNEL experiment and flow cytometry. Xenograft tumor assays in BALB/c nude mice confirmed that SMPDL3A promoted tumor growth and in vivo. Preliminary exploration of SMPDL3A interacting protein by mass spectrometry analysis and co-immunoprecipitation. Results: This study showed that the expression of SMPDL3A in HCC tissue differed from that in tumor-adjacent tissues. Moreover, the overall survival rate and tumor-free survival rate of patients with high-SMPDL3A expression were significantly lower than those with low-SMPDL3A expression. SMPDL3A expression was closely related to the level of protein induced by PIVKA-II, liver cirrhosis, tumor diameter, microvascular invasion, and Barcelona clinic liver cancer staging. Thus, SMPDL3A is an independent risk factor that affects the tumor-free survival rate and overall survival rate of HCC patients. In vitro study using Crispr-Cas9 genome editing technology revealed the knockout effect of SMPDL3A on cell proliferation, apoptosis, and migration. Cell counting kit-8 assay and clone formation experiment showed that sgSMPDL3A inhibited tumor cell proliferation and migration. Flow cytometry and TUNEL assay showed that sgSMPDL3A promoted apoptosis in tumors. Moreover, sgSMPDL3A inhibited tumor growth during subcutaneous tumor formation in nude mice. Immunohistochemistry of Ki67 and PNCA also indicated that sgSMPDL3A inhibited subcutaneous tumor proliferation in tumor-bearing nude mice. Further experiments showed that SMPDL3A interacts with the enhancer of rudimentary homolog (ERH). Conclusions: High-SMPDL3A expression was related to poor prognosis of patients with HCC. Knockout of SMPDL3A inhibited the proliferation and migration and accelerated the migration of HCC cells. SMPDL3A interacted with ERH to affect the tumorigenesis and progression of HCC.

Dataset Information

Transcription profiling of mouse liver from p53-/- animals with Ad TRF2DBDM compared to Ad GFP (2x10^10 PFU) (GSM103546, GSM103547) to investigate telomere dysfunction

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