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Expression data from Merm1/Wbscr22 knock-down tumor cells

ABSTRACT: Merm1/Wbscr22 is one of genes in chromosomal region deleted in Williams-Beuren syndrome, a multisystem developmental disorder. Wbscr22 contains a nuclear localization signal and an S-adenosyl-L-methionine-dependent methyltransferase fold, but its real function is completely unknown.　In this study, to examine the function, we compared the gene expression profiles between control and Merm1/Wbscr22 knock-downed tumor cells. Four established cell lines were selected for RNA extraction and hybridization on Affymetrix microarrays: (1) control LM8 cells, designated as LM8/control, (2) Merm1/Wbscr22 knock-downed LM8 cells, designated as LM8/shRNA, (3) control A375M cells, designated as A375M/control, and (4) Merm1/Wbscr22 knock-downed A375M cells, designated as A375M/shRNA.

ORGANISM(S): Homo sapiens

SUBMITTER: Nakazawa Youya

PROVIDER: S-ECPF-GEOD-22065 | biostudies-other |

REPOSITORIES: biostudies-other

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Expression data from Merm1/Wbscr22 knock-down tumor cells

Project description:Expression data from Merm1/Wbscr22 knock-down tumor cells

| PRJNA127485 | ENA

Expression data from Merm1/Wbscr22 knock-down tumor cells

2010-09-01 | GSE22065 | GEO

Rapid conditional knock-down-knock-in system for mammalian cells.

Project description:RNA interference (RNAi) is a powerful tool to analyze gene function in mammalian cells. However, the interpretation of RNAi knock-down phenotypes can be hampered by off-target effects or compound phenotypes, as many proteins combine multiple functions within one molecule and coordinate the assembly of multimolecular complexes. Replacing the endogenous protein with ectopic wild-type or mutant forms can exclude off-target effects, preserve complexes and unravel specific roles of domains or modifications. Therefore, we developed a rapid-knock-down-knock-in system for mammalian cells. Stable polyclonal cell lines were generated within 2 weeks by simultaneous selection of two episomal vectors. Together these vectors mediated reconstitution and knock-down in a doxycycline-dependent manner to allow the analysis of essential genes. Depletion was achieved by an artificial miRNA-embedded siRNA targeting the untranslated region of the endogenous, but not the ectopic mRNA. To prove effectiveness, we tested 17 mutants of WDR12, a factor essential for ribosome biogenesis and cell proliferation. Loss-off function phenotypes were rescued by the wild-type and six mutant forms, but not by the remaining mutants. Thus, our system is suitable to exclude off-target effects and to functionally analyze mutants in cells depleted for the endogenous protein.

| S-EPMC1807947 | biostudies-literature

Expression data from Merm1/Wbscr22 knock-down tumor cells

Project description:Merm1/Wbscr22 is one of genes in chromosomal region deleted in Williams-Beuren syndrome, a multisystem developmental disorder. Wbscr22 contains a nuclear localization signal and an S-adenosyl-L-methionine-dependent methyltransferase fold, but its real function is completely unknown.　In this study, to examine the function, we compared the gene expression profiles between control and Merm1/Wbscr22 knock-downed tumor cells. Four established cell lines were selected for RNA extraction and hybridization on Affymetrix microarrays: (1) control LM8 cells, designated as LM8/control, (2) Merm1/Wbscr22 knock-downed LM8 cells, designated as LM8/shRNA, (3) control A375M cells, designated as A375M/control, and (4) Merm1/Wbscr22 knock-downed A375M cells, designated as A375M/shRNA.

2010-09-01 | E-GEOD-22065 | biostudies-arrayexpress

Expression data from transformed WT and HGPS cell lines, including HGPS cells after knock-down of BRD4

Project description:Primary skin fibroblasts from a HGPS patient and an age-matched control wild-type individual were challenged in a standard transformation assay by retroviral introduction of TERT (T), V12-HRAS (R) and SV40 large and small T antigens (S). Knock-down of BRD4 in this TRS-HGPS cell line (TRS-HGPS-shBRD4) was achieved by retroviral introduction of independent shRNAs (shBRD4-1 to -3) Abstract: Advanced age and DNA damage accumulation are strong risk factors for cancer. The premature-aging disorder Hutchinson Gilford Progeria Syndrome (HGPS) provides a unique opportunity to study the interplay between DNA damage and aging-associated tumor mechanisms, since HGPS patients do not develop tumors despite elevated levels of DNA damage. Here, we have used HGPS patient cells to identify a protective mechanism to oncogenesis. We find that HGPS cells are resistant to neo-plastic transformation. This resistance is mediated by the bromodomain protein BRD4, which exhibits altered genome-wide binding patterns in transformation-resistant cells leading to inhibition of oncogenic de-differentiation. BRD4 also in-hibits, albeit to a lower extent, the tumorigenic potential of transformed cells from healthy individuals and BRD4-mediated tumor protection is clinically relevant, since a BRD4 gene signature predicts positive clinical outcome in breast and lung cancer. Our results demonstrate a protective function for BRD4 and suggest tissue-specific functions for BRD4 in tumorigenesis. 2 biological replicates are included for TRS-WT and TRS-HGPS cell lines. 3 biological replicates are included for TRS-HGPS-shBRD4 (derived from 3 independent shRNAs against BRD4)

| S-ECPF-GEOD-60519 | biostudies-other

Gene expression profile of Hodgkin?s lymphoma cells after knock-down of PRAME

Project description:By using high-density DNA microarrays, we analyzed the gene-expression profile of Hodgkin's lymphoma cell line L-428 after knock-down of the tumor antigen PRAME (preferentially expressed antigen in melanoma) Kewitz and Staege, submitted RNA was extracted from established Hodgkin's lymphoma cell line L-540 and hybridized with Affymetrix HG_U133A microarrays.

| S-ECPF-GEOD-40988 | biostudies-other

Gene expression of T47D-MTVL human breast cancer cells upon H1X knock-down

Project description:Gene expression of T47D-MTVL human breast cancer cells expressing Dox-inducible shRNAs against histone H1X Stable breast cancer-derived cell lines expressing an shRNA against the histone H1X isoforms in response to doxycycline (Dox) were grown for six days in the presence or absence of Dox, and serum-starved for the last 48h for synchronization in G1, in duplicate, and RNA extracted for microarray hybridization. Cell lines used: inducible shRNA against H1X, and random shRNA-expression vector as a control.

| S-ECPF-GEOD-62766 | biostudies-other

Expression data from Rad21 knock-down in ES cells

Project description:The Cohesin complex has recently been described to regulate gene expression. We wanted to determine the gene expression profile specific in mouse ES cells after depletion of the Cohesin subunit Rad21. We used microarrays to detail the global programme of gene expression underlying depletion of Rad21 and identified distinct early development related genes up-regulated and many pluripotency related genes downregulated.

2011-05-19 | GSE23923 | GEO

Knock-down of NDRG2 sensitizes cervical cancer Hela cells to cisplatin through suppressing Bcl-2 expression.

Project description:BACKGROUND: NDRG2, a member of N-Myc downstream regulated gene family, plays some roles in cellular stress, cell differentiation and tumor suppression. We have found that NDRG2 expression in cervical cancer Hela cells increases significantly upon stimulation with cisplatin, the most popular chemotherapeutic agent currently used for the treatment of advanced cervical cancer. This interesting phenomenon drove us to evaluate the role of NDRG2 in chemosensitivity of Hela cells. METHODS: In the present study, RNA interference was employed to down-regulate NDRG2 expression in Hela cells. RT-PCR and Western blot were used to detect expression of NDRG2, Bcl-2 and Bax in cancer cells. Real-time PCR was applied to detect miR-15b and miR-16 expression levels. Drug sensitivity was determined with MTT assay. Cell cloning efficiency was evaluated by Colony-forming assay. Apoptotic cells were detected with annexin V staining and flow cytometry. RESULTS: In vitro drug sensitivity assay revealed that suppression of NDRG2 could sensitize Hela cells to cisplatin. Down-regulation of NDRG2 didn't influence the colony-forming ability but promoted cisplatin-induced apoptosis of Hela cells. Inhibition of NDRG2 in Hela cells was accompanied by decreased Bcl-2 protein level. However, Bcl-2 mRNA level was not changed in Hela cells with down-regulation of NDRG2. Further study indicated that miR-15b and miR-16, two microRNAs targetting Bcl-2, were significantly up-regulated in NDRG2-suppressed Hela cells. CONCLUSIONS: These data suggested that down-regulation of NDRG2 could enhance sensitivity of Hela cells to cisplatin through inhibiting Bcl-2 protein expression, which might be mediated by up-regulating miR-15b and miR-16.

| S-EPMC3493279 | biostudies-literature

Gene expression of T47D-MTVL human breast cancer cells upon H1.4 knock-down or overexpression

Project description:Gene expression of T47D-MTVL human breast cancer cells expressing Dox-inducible shRNAs against histone H1.4 (sh120) or multiple H1 variants (sh225), or overexpressing WT or K26A mutant HA-tagged H1.4. T47D-MTVL, breast cancer cell line carrying one stably integrated copy of luciferase reporter gene driven by the MMTV promoter, is stably infected with an inducible system for the expression of shRNAs.Cells stably express RedFP and KRAB repressor fused to Tet regulator.Upon Dox treatment, cells express RedFP and the cloned shRNA. Stable breast cancer-derived cell lines expressing an shRNA against one of each of the histone H1 isoforms in response to doxycycline (Dox) were grown for six days in the presence or absence of Dox, in duplicate, and RNA extracted for microarray hybridization. Cell lines used: inducible shRNA against H1.4 or multiple H1 variants, and random shRNA-expression vector. Stable breast cancer-derived cell lines expressing the histone H1.4 isoform, WT or K26A, HA-tagged, in duplicate, and RNA extracted for microarray hybridization. Cell lines used: overexpressing H1.4 WT or K26A mutant.

| S-ECPF-GEOD-55786 | biostudies-other

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