Expression of CDC5L is associated with tumor progression in gliomas

Wang

Journal of Biological Chemistry

et al. 2018

The brilliant cresyl blue (BCB) test is used in both basic biological research and assisted reproduction to identify oocytes likely to be developmentally competent. However, the underlying molecular mechanism targeted by the BCB test is still unclear. To explore this question, we first confirmed that BCB-positive porcine oocytes had higher rates of meiotic maturation, better rates of cleavage and development into blastocysts, and lower death rates. Subsequent single-cell transcriptome sequencing on porcine germinal vesicle (GV)-stage oocytes identified 155 genes that were significantly differentially expressed between BCB-negative and BCB-positive oocytes. These included genes such as ,, ,, ,, and , which are enriched in functionally important signaling pathways including cell cycle regulation, oocyte meiosis, spliceosome formation, and nucleotide excision repair. In BCB-positive GV oocytes that additionally had a lower frequency of DNA double-strand breaks, the CDC5L protein was significantly more abundant./CDC5L inhibition by short interference (si)RNA or antibody microinjection significantly impaired porcine oocyte meiotic maturation and subsequent parthenote development. Taken together, our single-oocyte sequencing data point to a potential new role for CDC5L in porcine oocyte meiosis and early embryo development, and supports further analysis of this protein in the context of the BCB test.

Section: Cdc5l and Oocyte Maturationmentioning

confidence: 99%

Single-cell transcriptome sequencing reveals that cell division cycle 5-like protein is essential for porcine oocyte maturation

Wang

Journal of Biological Chemistry

et al. 2018

“…Cell division cycle 5-like (CDC5L) is a cell cycle regulatory element of G2/M transformation and is involved in the catalytic steps of mRNA splicing and DNA damage repair. Studies indicated that CDC5L expression in glioma and hepatocellular carcinoma was increased, and CDC5L interference could increase the cell cycle arrest in G2 phase and inhibit the proliferation of glioma cells and hepatoma cells [15,16]. However, CDC5L has not been studied in MM.…”

Section: Introductionmentioning

confidence: 99%

ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L

Guo

Sha

et al. 2020

Aging

This study aimed to investigate whether annexin A7 (ANXA7) could promote the cell cycle, proliferation and cell adhesion-mediated drug resistance (CAM-DR) of multiple myeloma (MM) cells by up-regulating cell division cycle 5-like (CDC5L). As a result, ANXA7 expression was increased in the serum of MM patients and the expression of ANXA7 and CDC5L was also increased in MM cell lines. ANXA7 overexpression promoted the proliferation and cycle of U266 and RPMI8226 cells. The expression of proliferation cell nuclear antigen (PCNA), KI67, cyclin dependent kinase 1 (CDK1) and cyclinB1 in transfected cells was consistent with the changes of proliferation and cell cycle. In co-culture system of BMSC cells and MM cells, expression of CD44, ICAM1 and VCAM1 in MM cells was increased, which was further increased by ANXA7 overexpression. Bortezomib could increase the apoptosis of U266 and RPMI8226 cells. In co-culture system of BMSC cells and MM cells, the promotion effects of bortezomib on apoptosis of MM cells was decreased, which was further suppressed by ANXA7 overexpression. The above effects exerted by ANXA7 overexpression could be reversed by ANXA7 interference. Moreover, ANXA7 was proved to be combined with CDC5L. CDC5L interference could inhibit the promotion effects of ANXA7 overexpression on proliferation and cell cycle and inhibition effects of ANXA7 overexpression on apoptosis of MM cells treated with bortezomib in co-culture system. In conclusion, ANXA7 could promote the cell cycle, proliferation and CAM-DR of MM cells by upregulating CDC5L.

“…In the current gene signature list, CDC5L is correlated with advanced TNM stage of osteosarcoma ( 25 ) and responds poorly to neo-adjuvant chemotherapy ( 26 ). Overexpression of CDC5L favors cell cycle progression of hepatocellular carcinoma cells ( 27 ) and also plays an important role in glioma ( 28 ). TGFBR2 might be a key gene associated with sarcoma ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Predicting radiotherapy response for patients with soft tissue sarcoma by developing a molecular signature

Tang

Zeng

et al. 2017

Oncology Reports

Soft tissue sarcomas are rare and aggressive tumors arising from connective tissues. Adjuvant radiotherapy is a commonly used treatment approach for the majority of sarcomas. We attempted to identify a gene signature that can predict radiosensitive patients who are most likely to have a better treatment response from radiotherapy, compared with disease progression. Using the publicly available data of soft tissue sarcoma from The Cancer Genome Atlas, we developed a cross-validation procedure to identify a predictive gene signature for radiosensitivity. The results showed that the predicted radiosensitive patients who received radiotherapy had significantly improved treatment response. We further provide supportive evidence to validate our sensitivity prediction. Results showed that the predicted radiosensitive patients who received radiotherapy had significantly improved survival than patients who did not. ROC analysis showed that the developed gene signature had a powerful prediction on treatment response. We further found that predicted radiosensitive patients who received radiotherapy had a significantly reduced rate of new tumor events. Finally, we validated our gene signature using a hierarchical cluster analysis, and found that the predicted sensitivities were well-matched with results from the cluster analysis. These results are consistent with our expectation, suggesting that the identified gene signature and radiosensitivity prediction are effective. The genes involved in the signature may provide a molecular basis for prognostic studies and radiotherapy target discovery.