The suppression of DUSP5 expression correlates with paclitaxel resistance and poor prognosis in basal-like breast cancer

Liu, Tieju; Sun, Hongxia; Liu, Shiqi; Zhao, Yupei; Li, Linqi; Yao, Nan; Cheng, Siqi; Dong, Xueyi; Liang, Xiaohui; Chen, Chen; Wang, Yi; Zhao, Xiulan

doi:10.7150/ijms.24981

Cited by 20 publications

(13 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Further, phosphatases such as ALPL and PTP4A3, which are increased in late-stage and aggressive triple-negative breast cancers, have been found to be indicative of poor patient survival and have been discovered to be promoters of cancer cell proliferation (Singh et al, 2013;den Hollander et al, 2016). Importantly, suppression of DUSP5 expression is correlated with paclitaxel resistance and poor prognosis in basal-like breast cancer (Liu et al, 2018). Fig.…”

Section: Ampk Phosphorylation Potentiates Taxol Cytotoxicitymentioning

confidence: 99%

Cyclin-dependent kinase 1-mediated AMPK phosphorylation regulates chromosome alignment and mitotic progression

Stauffer

Zeng

Santos

et al. 2019

Journal of Cell Science

View full text Add to dashboard Cite

AMP-activated protein kinase (AMPK), a heterotrimeric serine/ threonine kinase and cellular metabolic sensor, has been found to regulate cell cycle checkpoints in cancer cells in response to energetic stress, to harmonize proliferation with energy availability. Despite AMPK's emergent association with the cell cycle, it still has not been fully delineated how AMPK is regulated by upstream signaling pathways during mitosis. We report, for the first time, direct CDK1 phosphorylation of both the catalytic α1 and α2 subunits, as well as the β1 regulatory subunit, of AMPK in mitosis. We found that AMPKknockout U2OS osteosarcoma cells have reduced mitotic indexes and that CDK1 phosphorylation-null AMPK is unable to rescue the phenotype, demonstrating a role for CDK1 regulation of mitotic entry through AMPK. Our results also denote a vital role for AMPK in promoting proper chromosomal alignment, as loss of AMPK activity leads to misaligned chromosomes and concomitant metaphase delay. Importantly, AMPK expression and activity was found to be critical for paclitaxel chemosensitivity in breast cancer cells and positively correlated with relapse-free survival in systemically treated breast cancer patients.

show abstract

Section: Ampk Phosphorylation Potentiates Taxol Cytotoxicitymentioning

confidence: 99%

Cyclin-dependent kinase 1-mediated AMPK phosphorylation regulates chromosome alignment and mitotic progression

Stauffer

Zeng

Santos

et al. 2019

Journal of Cell Science

View full text Add to dashboard Cite

show abstract

“…Chemotherapy is a basic strategy for treating breast cancer ( 3 , 4 ), however, this approach has several limitations, including limited drug delivery due to the blood-brain barrier and drug resistance ( 5 , 6 ). Paclitaxel, as one of the most effective chemotherapeutic drugs, is used to treat breast cancer ( 7 , 8 ), however, its failure in treatment and poor prognosis are mainly due to the development of drug resistance ( 9 ).…”

Section: Introductionmentioning

confidence: 99%

NT21MP negatively regulates paclitaxel-resistant cells by targeting miR‑155‑3p and miR‑155-5p via the CXCR4 pathway in breast cancer

et al. 2018

View full text Add to dashboard Cite

Evidence has shown that microRNAs (miRNAs) are vital in cell growth, migration, and invasion by inhibiting their target genes. A previous study demonstrated that miRNA (miR)-155-3p and miR-155-5p exerted opposite effects on cell proliferation, apoptosis, migration and invasion in breast cancer cell lines. An miRNA microarray was used to show that miR-155-3p was downregulated whereas miR-155-5p was upregulated in paclitaxel-resistant (PR) cells compared with parental breast cancer cells. However, the role of miR-155 in breast cancer cell invasion and metastasis remains to be elucidated. A 21-residue peptide derived from the viral macrophage inflammatory protein II (NT21MP), competes with the ligand of CXC chemokine receptor 4 (CXCR4) and its ligand stromal cell-derived factor-1α, inducing cell apoptosis in breast cancer. The present study aimed to identify the underlying mechanism of action of miR-155-3p/5p and NT21MP in PR breast cancer cells. Quantitative polymerase chain reaction, western blotting, wound-healing, cell cycle and apoptosis assays, and Cell Counting kit-8 assay were used to achieve this goal. The combined overexpression of miR-155-3p with NT21MP decreased the migration and invasion ability and increased the number of apoptotic and arrested cells in the G0/G1 phase transition in vitro. The knockdown of miR-155-5p combined with NT21MP had a similar effect on PR breast cancer cells. Furthermore, the ectopic expression of their target gene myeloid differentiation primary response gene 88 (MYD88) or tumor protein 53-induced nuclear protein 1 (TP53INP1) combined with NT21MP enhanced the sensitivity of the breast cancer cells to paclitaxel. Taken together, these findings suggested that miR-155-3p/5p and their target genes MYD88 and TP53INP1 may serve as novel biomarkers for NT21MP therapy through the CXCR4 pathway for improving sensitivity to paclitaxel in breast cancer.

show abstract

“…As our data shows, the protein level of DUSP5 is reduced with HPV 16E7 overexpressing. And several studies showed that suppression of DUSP5 expression correlates with cancer cell proliferation, migration, invasion and poor prognosis in different cancer types (Liu et al, 2018;Wang et al, 2019;Du et al, 2020), but the relationship between DUSP5 and HPV has thus far remained undiscovered. Therefore, these genes may be the candidates for further studies.…”

Section: Discussionmentioning

confidence: 99%

Digital RNA Sequencing of Human Epidermal Keratinocytes Carrying Human Papillomavirus Type 16 E7

et al. 2020

View full text Add to dashboard Cite

High-risk human papillomavirus (HPV) infections are the predominant cause of cervical cancer and its early gene E7 plays an important role in cellular proliferation and cell-cycle progression. While tremendous progress has been made in exploring the molecular mechanisms in late tumorigenesis, many pathways showing how HPV deregulates host gene expression in early inapparent infections and early tumorigenesis still remain undefined. Digital RNA sequencing was performed and a total of 195 differentially expressed genes were identified between the HPV16 E7-transfected NHEKs and control cells (p < 0.05, fold-change > 2). GO enrichment showed that HPV16 E7 primarily affected processes involved in anti-viral and immune responses, while KEGG pathway analysis showed enrichment of gene clusters of associated with HPV infection and MAPK signaling. Of the differentially expressed genes, IFI6, SLC39A9 and ZNF185 showed a strong correlation with tumor progression and patient survival in the OncoLnc database while roles for AKAP12 and DUSP5 in carcinogenesis and poor prognosis have previously been established for other cancer types. Our study identified several novel HPV16 E7-regulated candidate genes with putative functions in tumorigenesis, thus providing new insights into HPV persistence in keratinocytes and early onset of tumorigenesis.

show abstract

The suppression of DUSP5 expression correlates with paclitaxel resistance and poor prognosis in basal-like breast cancer

Cited by 20 publications

References 29 publications

Cyclin-dependent kinase 1-mediated AMPK phosphorylation regulates chromosome alignment and mitotic progression

Cyclin-dependent kinase 1-mediated AMPK phosphorylation regulates chromosome alignment and mitotic progression

NT21MP negatively regulates paclitaxel-resistant cells by targeting miR‑155‑3p and miR‑155-5p via the CXCR4 pathway in breast cancer

Digital RNA Sequencing of Human Epidermal Keratinocytes Carrying Human Papillomavirus Type 16 E7

Contact Info

Product

Resources

About