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DNA polymerase POLD1 promotes proliferation and metastasis of bladder cancer by stabilizing MYC

ABSTRACT: DNA polymerase POLD1 promotes proliferation and metastasis of bladder cancer by stabilizing MYC

PROVIDER: PRJNA827152 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18771370_1.fastq.gz	Fastqsanger.gz
	SRR18771370_2.fastq.gz	Fastqsanger.gz
	SRR18771371_1.fastq.gz	Fastqsanger.gz
	SRR18771371_2.fastq.gz	Fastqsanger.gz
	SRR18771372_1.fastq.gz	Fastqsanger.gz

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DNA polymerase POLD1 promotes proliferation and metastasis of bladder cancer by stabilizing MYC

Project description:Hitherto, most studies on POLD1 have mainly focused on the effect of POLD1 inactivation mutation in tumors. Nonetheless, the mechanism underlying high POLD1 expression in tumorigenesis remains elusive. Herein, we substantiated the pro-carcinogenic role of POLD1 in bladder cancer (BLCA) and found that POLD1 expression is related to malignancy and prognosis of BLCA. Next, we demonstrated that POLD1 could promote proliferation and metastasis of BLCA via MYC. Mechanistically, we demonstrated that POLD1 was able to stabilize MYC in a manner independent of DNA polymerase activity. POLD1 attenuated the FBXW7-mediated ubiquitination degradation of MYC by directly binding to the MYC homology box 1 domain competitively with FBXW7. Moreover, we found that POLD1 can form a complex with MYC to promote the transcriptional activity of MYC. MYC could also transcriptionally activate POLD1, forming a POLD1-MYC positive feedback loop to enhance the pro-carcinogenic effect of POLD1-MYC on BLCA. Overall, our study suggests a novel MYC-driven mechanism for BLCA, and POLD1 has the potential as a biomarker for BLCA.

2023-03-29 | PXD040806 | Pride

DNA polymerase POLD1 promotes proliferation and metastasis of bladder cancer by stabilizing MYC

Project description:Hitherto, most studies on DNA polymerase δ (POLD1) have mainly focused on the effect of POLD1 inactivation mutation in tumors. Nonetheless, the mechanism underlying high POLD1 expression in tumorigenesis remains elusive. Herein, we substantiated the pro-carcinogenic role of POLD1 in bladder cancer (BLCA) and found that POLD1 expression is related to malignancy and prognosis of BLCA. Next, we demonstrated that POLD1 could promote proliferation and metastasis of BLCA via MYC in vivo and in vitro. Furthermore, POLD1 and MYC were colocalized in the nucleus and co-expressed during the cell cycle. Mechanistically, we validated that POLD1 could interact directly with MYC, and POLD1 could stabilize MYC by counteracting GSK3β-mediated phosphorylation of threonine 58 and blocking the interaction between E3 ubiquitin ligase FBXW7 and MYC. Moreover, MYC could transcriptionally activate POLD1, forming a POLD1-MYC positive feedback loop to enhance the pro-carcinogenic effect of POLD1-MYC on BLCA. Overall, our study identified a novel MYC-driven oncogene POLD1, providing a potential diagnostic and therapeutic target for BLCA.

2022-04-22 | GSE200897 | GEO

Deubiquitinase USP20 promotes breast cancer metastasis by stabilizing SLUG

Project description:Deubiquitinase USP20 promotes breast cancer metastasis by stabilizing SLUG

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m5C Promotes Pathogenesis of the Bladder Cancer Through Stabilizing mRNAs

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CircNCOR1 suppresses lymphatic metastasis in bladder cancer

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miR-193 inhibits bladder cancer progression by targeting N-myc

Project description:Growing evidence has indicated that miR-193 is involved in the initiation and progression of malignancy, such as bladder cancer, hepatocellular carcinoma, renal cell carcinoma, and colorectal cancer. Nevertheless, the mechanisms of miR-193 in the development of metastatic bladder cancer remains unknown. In the current study, we clarified the association of miR-193/N-myc was implicated in cancer metastasis. miR-193 expression increased in metastatic bladder cancer biopsies compared to the primary cases. Moreover, the elevation of miR-193 was correlated with the invasiveness, lymph node metastasis, and advanced stages of bladder cancer significantly. Downregulation of miR-193 by shRNA hampered proliferation and migration while inducing cell apoptosis. Furthermore, miR-193 sponged N-myc and diminished miR-103 expression. Overexpression of miR-193 released oncogene N-myc expression, leading to the promotion of cell proliferation and migration. Besides, knockout of miR-193 suppressed tumor growth in the human T24 mice models. Briefly, the present findings suggested that miR-193-N-myc were novel promising pathways for conquering bladder cancer progression.

2021-01-13 | GSE164682 | GEO

exosomal ELNAT1 promotes lymphatic metastasis of bladder cancer

Project description:The crosstalk between tumor cells and LECs triggers the LN metastasis in bladder cancer (BCa), but the underlying mechanisms are not completely understood. Previously, we identified that BCa-secreted extracellular vesicles (EVs)-packaged lncRNAs mediated the communication with LECs and promoted LN metastasis. To evaluate whether EV-packaged lncRNAs triggered the LN metastasis of BCa, next-generation sequencing (NGS) to the global expression profiles of lncRNAs was utilized in the urinary EVs (urinary-EV) of five MIBC patients and five healthy volunteers.

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Targeting TIGIT Molecule Inhibits the Metastasis of Bladder Cancer through Suppressing IL-32

Project description:Bladder cancer is a highly metastatic tumor and one of the most common malignant tumors originating in the urinary system. Although the application of immune checkpoint, including programmed cell death-1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), achieved definite efficacy, the effect of immunotherapy for bladder cancer is still not very satisfactory. Therefore, it is very urgent to develop new targets to expand the options of immunotherapies. In this study, we utilized single cell sequencing to explore the cell composition and detected a subset of Treg cells with high expression of T cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT) and interleukin (IL)-32 molecules. Certainly, anti-tumor immune response was suppressed by this subset of Treg cells and IL-32 promoted the bladder cancer metastasis. Nevertheless, targeting TIGIT not only could reverse immunosuppression through restoring anti-tumor immune response mediated by T cells but suppressed the secretion of IL-32 and inhibited the metastasis of bladder cancer cells. Thus, our study provided a novel insight into the immunosuppression in bladder cancer and developed the TIGIT as the novel target for immunotherapy of bladder cancer. Furthermore, we also illustrated mechanism of the dual effect of targeting TIGIT in bladder cancer and revealed the metastasis-promoting effect of IL-32 in bladder cancer. Taken together, the discovery raises the possibility of TIGIT targets against bladder cancer from the bench to the bedside.

2022-01-31 | GSE186520 | GEO

exosomal ELNAT1 promotes lymphatic metastasis of bladder cancer

Project description:exosomal ELNAT1 promotes lymphatic metastasis of bladder cancer

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Long noncoding RNA LNMAT1 promotes lymphatic metastasis in bladder cancer

Project description:Long non-coding RNAs (lncRNAs) are a large class of non-protein-coding transcripts that are over 200nt in length. LncRNAs have emerged as key regulator of biological process involved in the development and progression of bladder cancer. Bladder cancer is one of the most common genitourinary malignancies worldwide, with approximately 429,800 new cases and 165,100 deaths annually in the world. To identify critical lncRNAs that contributes to the progression of bladder cancer, Next generation sequencing (NSG) was performed in five paired high-grade muscle invasive bladder cancer (MIBC) and normal adjacent tissues (NAT), and in five lymph node (LN)-positive and LN-negative bladder cancer tissues. Our results indicate that the differential expressed lncRNAs in both MIBC tissues and LN-positive tissues associated in a variety of biological functions, such as metastasis.

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