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LAPTM4B-YAP loop feedback amplification enhances the stemness of hepatocellular carcinoma

ABSTRACT: LAPTM4B-YAP loop feedback amplification enhances the stemness of hepatocellular carcinoma

PROVIDER: PRJNA953402 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24107313_1.fastq.gz	Fastqsanger.gz
	SRR24107313_2.fastq.gz	Fastqsanger.gz
	SRR24107314_1.fastq.gz	Fastqsanger.gz
	SRR24107314_2.fastq.gz	Fastqsanger.gz
	SRR24107315_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

LAPTM4B-YAP loop feedback amplification enhances the stemness of hepatocellular carcinoma

Project description:To investigate the function of LAPTM4B in the regulation of stemness, we established CD133+ HepG2 cells with or without knocked down LAPTM4B.

2023-04-11 | GSE229205 | GEO

LAPTM4B-YAP loop feedback amplification enhances the stemness of hepatocellular carcinoma.

Project description:Hepatocellular carcinoma (HCC) is highly heterogeneous, and stemness signatures are frequently elevated in HCC tumor cells to generate heterogeneous subtypes via multidirectional differentiation. However, the mechanisms affecting the regulation of stemness in HCC remain unclear. In this study, we identified that lysosome-associated protein transmembrane-4β (LAPTM4B) was significantly overexpressed in stem-like tumor cell populations with multidirectional differentiation potential at the single cell level, and verified that LAPTM4B was closely related to stemness of HCC using in vitro and in vivo experiments. Mechanistically, elevated LAPTM4B suppresses Yes-associated protein (YAP) phosphorylation and ubiquitination degradation. In turn, stabilized YAP localizes to the nucleus and binds to cAMP responsive element binding protein-1 (CREB1), which promotes transcription of LAPTM4B. Overall, our findings suggest that LAPTM4B forms a positive feedback loop with YAP, which maintains the stemness of HCC tumor cells and leads to an unfavorable prognosis for HCC patients.

| S-EPMC10197148 | biostudies-literature

CCN2-MAPK-Id-1 Loop Feedback Amplification is involved in Maintaining Stemness in Oxaliplatin-resistant Hepatocellular Carcinoma

Project description:CCN2-MAPK-Id-1 Loop Feedback Amplification is involved in Maintaining Stemness in Oxaliplatin-resistant Hepatocellular Carcinoma

| PRJNA512377 | ENA

ABHD5 inhibits YAP-induced c-Met overexpression and colon cancer cell stemness via suppressing YAP methylation

Project description:Cancer stemness represents a major source of development and progression of colorectal cancer (CRC). c-Met critically contributes to CRC stemness, but how c-Met is activated in CRC remains elusive. We previously identified the lipolytic factor ABHD5 as an important tumour suppressor gene in CRC. Here, we show that loss of ABHD5 promotes c-Met activation to sustain CRC stemness in a non-canonical manner. Mechanistically, we demonstrate that ABHD5 interacts in the cytoplasm with the core subunit of the SET1A methyltransferase complex, DPY30, thereby inhibiting the nuclear translocation of DPY30 and activity of SET1A. In the absence of ABHD5, DPY30 translocates to the nucleus and supports SET1A-mediated methylation of YAP and histone H3, which sequesters YAP in the nucleus and increases chromatin accessibility to synergistically promote YAP-induced transcription of c-Met, thus promoting the stemness of CRC cells. This study reveals a novel role of ABHD5 in regulating histone/non-histone methylation and CRC stemness. We used microarrays to detail the gene expression of HCT116 colon cancer cell and ABHD5 knockdown HCT116 cell.

2021-11-24 | GSE185056 | GEO

CCN2-MAPK-Id-1 Loop Feedback Amplification is involved in Maintaining Stemness in Oxaliplatin-resistant Hepatocellular Carcinoma

Project description:Hepatocellular carcinoma (HCC) is the second leading cause of cancer death worldwide. Most patients are at an advanced stage at diagnosis, and are not eligible for curative therapy. Chemotherapy is an alternative treatment for advanced HCCs, but resistance is found in many patients. Understanding the underlying mechanisms in chemo-resistance is critical to further improve the efficacy of HCC treatment. In this study, we found that increased expression of Id-1 and CCN2 were closely related to oxaliplatin resistance in HCC. Upregulation of CCN2 and Id-1 was independently associated with shorter survival and increased recurrence in HCC patients, and significantly enhanced oxaliplatin resistance and promoted lung metastasis in vivo, whereas knock-down of their expression significantly reversed the chemo-resistance and inhibited HCC cell stemness. cDNA microarrays and PCR revealed that Id-1 and MAPK pathway were the downstream signaling of CCN2, and Id-1 could upregulate CCN2 in a positive feedback manner. Moreover, CCN2 significantly enhanced oxaliplatin resistance by activating the MAPK signaling pathway and upregulating Id-1 expression. Meanwhile, MAPK/Id-1 signaling was demonstrated as one of the most important autocrine signaling pathways regulated by CCN2 in oxaliplatin-resistant models, and combination with sorafenib could improve the efficacy of oxaliplatin in HCC. Conclusions: These findings suggest that CCN2-MAPK-Id-1 loop feedback amplification is involved in oxaliplatin-resistant HCC, and the combination of oxaliplatin with inhibitor of CCN2 or MAPK signaling could provide a promising approach to ameliorating HCC progression and oxaliplatin resistance.

2019-01-02 | GSE124529 | GEO

Gene expression profiling of Calu-6 lung cancer cells transfected with scrambled siRNA and LAPTM4B-specific siRNA

2016-08-01 | GSE66606 | GEO

Gene expression profiling of Calu-6 lung cancer cells transfected with scrambled siRNA and LAPTM4B-specific siRNA

Project description:We recently characterized the adjacent airway field of cancerization in NSCLC by whole transcriptome expression analysis and demonstrated that lysosomal protein transmembrane 4 beta (LAPTM4B) was an elevated field cancerization marker in NSCLCs and in adjacent but not in distant normal-appearing airways. We also found that LAPTM4B was up-regulated in NSCLCs compared to normal lung and promoted anchorage-dependent growth of lung cancer cells. Previous reports suggested that LAPTM4B is activated following metabolic and genotixc stress. The precise role of LAPTM4B in lung cancer cell survival and NSCLC pathogenesis is still elusive. In the present study we sought to examine how LAPTM4B expression levels impact downstream expression profiles and cell signaling in order to gain better insights into the function of this putative oncogene in lung cancer. Calu-6 lung cancer cells were transfected with SMARTpool (Dharmacon)control/scrambled siRNA or siRNA targeting LAPTM4B. Following transfection, cells were cultured in the presence or absence of 10% fetal bovine serum (FBS). Three independent transfections for each condition were performed representing three biological replicates per condition (total number of samples = 12). RNA interference-mediated knock-down of LAPTM4B in samples was confirmed by quantitative real-time PCR. Total RNA was profiled using the Human Gene 1.0 ST platform.

2016-08-01 | E-GEOD-66606 | biostudies-arrayexpress

YTHDF2-KIF26B-Wnt signaling forms a positive-feedback regulatory loop to maintain ISC stemness

Project description:m6A modification plays a regulatory role in the stemness of small intestinal epithelial stem cells (ISCs), which is crucial for the renewal of intestinal epithelium and the maintenance of homeostasis. Although existing research has demonstrated that METTL3, as an m6A ‘writer’, is a crucial protein in the regulation of the stemness of ISCs, the mechanism by which the function of downstream ‘reader’ proteins is regulated has not been fully elucidated. In this study, we found that the knockout of Ythdf2 could significantly down-regulate the expression of the stemness marker gene Lgr5, suggesting that this ‘reader’ protein plays an important role in the regulation of the stemness of ISCs. Upon exploring the specific downstream mechanisms, we discovered that YTHDF2 promoted the Wnt signaling pathway by regulating the expression of KIF26B. This helps maintain the expression of Lgr5 in stem cells, thus preserving the stemness of these cells. Meanwhile, the expression of YTHDF2 itself is also regulated by the Wnt signaling pathway. Overall, YTHDF2 forms a positive-feedback regulatory loop centered around the Wnt signaling pathway. This loop ensures that ISCs remain in a stem-cell state, enabling the intestinal epithelium to function stably and properly.

2025-05-12 | GSE290302 | GEO

ABHD5 inhibits YAP-induced c-Met overexpression and colon cancer cell stemness via suppressing YAP methylation

Project description:ABHD5 inhibits YAP-induced c-Met overexpression and colon cancer cell stemness via suppressing YAP methylation

| PRJNA767545 | ENA

α-Catenin Levels Determine Direction of YAP/TAZ Response to Autophagy Perturbation

Project description:The factors regulating cellular identity are critical for understanding the transition from health to disease and responses to therapies. Cell identity is generally assigned based on static phenotypes, like “omics” profiles. However, how such static features translate into dynamic responses to perturbations that determine cellular function is often unclear. We found that autophagy perturbation in different cell types can have opposite responses in growth-promoting oncogenic YAP/TAZ transcriptional signalling. These apparently contradictory responses can be resolved by a feedback loop where autophagy negatively regulates the levels of α-catenins LC3-interacting proteins, which inhibit YAP/TAZ, which, in turn, positively regulate autophagy. High basal levels of α-catenins enable autophagy induction to positively regulate YAP/TAZ, while low α-catenins cause YAP/TAZ activation upon autophagy inhibition. These data reveal how feedback loops enable post-transcriptional determination of cell identity and how levels of a single intermediary protein can dictate the direction of response to external or internal perturbations.

2021-03-19 | PXD023711 | Pride

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