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Identification of chemoresistant genes in hepatocellular carcinoma (HCC)

ABSTRACT: The aim of this study was to identify chemoresistance-associated genes in hepatocellular carcinoma (HCC). cDNA microarray analysis was performed to compare the mRNA expression profiles of a human metastatic HCC cell line (named MHCC97Low) and its derived chemoresistant sublines including cisplatin resistant subline (named MHCC97L/CisR or C8) and doxorubicin resistant subline (named MHCC97L/DoxR or D5).

ORGANISM(S): Homo sapiens

PROVIDER: GSE54175 | GEO | 2014/01/17

SECONDARY ACCESSION(S): PRJNA235336

REPOSITORIES: GEO

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Identification of chemoresistant genes in hepatocellular carcinoma (HCC)

Project description:The aim of this study was to identify chemoresistance-associated genes in hepatocellular carcinoma (HCC). cDNA microarray analysis was performed to compare the mRNA expression profiles of a human metastatic HCC cell line (named MHCC97Low) and its derived chemoresistant sublines including cisplatin resistant subline (named MHCC97L/CisR or C8) and doxorubicin resistant subline (named MHCC97L/DoxR or D5). Total RNAs were extracted from MHCC97Low (97Low as sample name), MHCC97L/CisR (C8 as sample name) and MHCC97L/DoxR (D5 as sample name), and hybridized on Affymetrix microarrays. We planed to identify differential genes between 97Low and C8 (cisplatin resistant genes) as well as to identify differential genes between 97Low and D5 (doxorubicin resistant genes).

2014-01-17 | E-GEOD-54175 | biostudies-arrayexpress

Expression data comparing chemoresistant (cisplatin and doxorubicin) hepatospheres and differentiated HCC cells

Project description:To identify candidate genes that are up-regulated in chemoresistant (cisplatin and doxorubicin) hepatospheres as compared with their differentiated counterparts Affymetrix Human Genome U133 Plus GeneChip 2.0 PLC/PRF/5 HCC cells were grown as spheroids and treated with cisplatin and doxorubicin combination. Differentiated counterparts were generated by addition of FBS in the spheroids and allowed to attach.

2014-06-01 | E-GEOD-53005 | biostudies-arrayexpress

Human BRAF-V600E melanoma cell lines drug sensitive vs drug resistant

Project description:aCGH of human melanoma cell lines comparing parental (drug sensitve) vs isogenic drug resistant-derived subline Two condition experiment: two BRAF-V600E mutant cell lines (drug sensitive - parental baseline) vs two derived sublines after chronic exposure to the MEK inhibitor trametinib (drug resistant) are compared

2014-04-21 | E-GEOD-49430 | biostudies-arrayexpress

Expression data comparing chemoresistant (cisplatin and doxorubicin) hepatospheres and differentiated HCC cells

2014-06-01 | GSE53005 | GEO

miR-1061 and miR-591 are involved in paclitaxel-resistance and their regulation increases the sensitivity to paclitaxel

Project description:MicroRNA expression in paclitaxel (PTX)-resistant SKpac sublines was compared to that of the PTX-sensitive, parental SKOV3 ovarian cancer cell line using microarray and real-time RT-PCR. The function of differentially expressed microRNAs in chemoresistant ovarian cancer was further evaluated by apoptosis, cell proliferation, and migration assays.

2013-01-17 | GSE43598 | GEO

miR-1061 and miR-591 are involved in paclitaxel-resistance and their regulation increases the sensitivity to paclitaxel

2013-01-17 | E-GEOD-43598 | biostudies-arrayexpress

Transcriptomic comparison of chemosensitive and chemoresistant cells

Project description:First, in a model of xenografts induced with HT-29 human colon cancer cells, we demonstrated that the transcription factor NF-kB was involved in the resistance to CPT-11. Then, from one tumor treated with CPT-11 plus a NF-kB inhibitor, we established a resistant cell line to CPT-11. The aim of this study was to compare the expression of genes involved in the signaling pathway of NF-kB between the sensitive and the resistant cell lines and to identify other genes (target or not of NF-kB) which the expression was modified when the resistant phenotype was acquired. Human colon cancer cells chemosensitive (HT-29) versus human colon cancer cells chemoresistant (RIV) in a dye-swap experiment.

2012-08-23 | E-GEOD-23433 | biostudies-arrayexpress

Gene expression profile of MX-1 breast cancer cell line and chemoresistant sublines of them

Project description:Breast cancer is a leading cause of cancer-related deaths among women in the Western world. Anthracyclines, including doxorubicin (DOX), along with taxanes, cyclophosphamide and platinum compounds are the main chemotherapeutic agents applied for breast cancer treatment. However, chemoresistance is the major cause of the disease progression following chemotherapy. Drug resistance can be either inherent or acquired during the treatment, but most possibly the interaction of both mechanisms drives the rapid development of treatment refractory cancer. In the present study, the mechanisms of acquired cellular chemoresistance were studied in breast cancer cell line MX-1 exposed to gradually increasing concentration of the chemotherapeutic compound DOX (MX-1/D). Nongenotoxic phosphorganic compound tetraphenylphosphonium cation (TPP+) – a potent substrate and activator for ABCB1 transporter – was used in the cell line model of intrinsic chemoresistance (MX-1/T). Finally, DOX highly resistant cell subline was derived from ABCB1-activated, TPP+ pretreated cells (MX-1/TD). Chemoresistance in all cell sublines was closely associated with the EMT, and the ABCB1 hyperexpression was a possibly trigger of this process.

2020-12-30 | GSE163986 | GEO

Enhancement of metastasis by spontaneous ploidy doubling of breast cancer cell MDA-MB-231.

Project description:MDA-MB-231 bone-metastatic subline 1833 and lung metastatic subline 4175 underwent spontaneous ploidy doubling in culture, i.e. the genome approximately duplicated itself gradually. The modal- and hyper-ploid subpopulations during the ploidy transition were sorted into two separate sublines, 1833-Modal and 1833-Hyper for 1833, 4175-Modal and 4175-Hyper for 4175. Their expresssion patterns were compared to each other as well as to other MDA-MB-231 sublines isolated previously by Kang et al. 2003 and Minn et al. 2005. Keywords: Cell type comparison 19 cell lines were analyzed, including the parental line MDA-MB-231, modal-ploid sublines 1833-Modal and 4175-Modal, hyper-ploid sublines 1833-Hyper and 4175-Hyper, strongly bone-metastatic lines 1833 (the original subline after short culture), 2274, 2268 and 2269, weakly bone-metastatic lines 2293, 2295 and 2297, strongly lung-metastaic lines 4142, 4173, 4175 (the original subline after short culture) and 4180, and weakly lung-metastatic lines SCP6, SCP21 and SCP26. Single sample for each line.

2010-06-08 | E-GEOD-16554 | biostudies-arrayexpress

Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma

Project description:Chemotherapy of retinoblastoma (RB), a malignant ocular childhood disease, is often limited by the development of resistances against commonly used drugs. We identified inositol polyphosphate 4-phosphatase type II (INPP4B) as a differentially regulated gene in etoposide resistant RB cell lines, potentially involved in the development of RB resistances. INPP4B is controversially discussed as a tumor suppressor and an oncogenic driver in various cancers, but its role in retinoblastoma in general and chemoresistant RB in particular is yet unknown. In the study presented, we investigated the expression of INPP4B in RB cell lines and patients and analyzed the effect of INPP4B overexpression on etoposide resistant RB cell growth in vitro and in vivo. INPP4B mRNA levels were significantly downregulated in RB cells lines compared to the healthy human retina, with even lower expression levels in etoposide resistant compared to the sensitive cell lines. Besides, a significant increase in INPP4B expression was observed in chemotherapy treated RB tumor patient samples compared to untreated tumors. INPP4B overexpression in etoposide resistant RB cells resulted in a significant reduction in cell viability with reduced growth, proliferation, anchorage-independent growth, and in ovo tumor formation. Caspase-3/7 mediated apoptosis was concomitantly increased, suggesting a tumor suppressive role of INPP4B in chemoresistant RB cells. No changes in AKT signalling were discernible, but p-SGK3 levels increased following INPP4B overexpression, indicating a potential regulation of SGK3 signalling in etoposide-resistant RB cells. RNAseq analysis of INPP4B overexpressing, etoposide resistant RB cell lines revealed differentially regulated genes involved in cancer progression, mirroring observed in vitro and in vivo effects of INPP4B overexpression and strengthening INPP4B`s importance for cell growth control and tumorigenicity.

2023-03-15 | GSE226408 | GEO

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