2020
DOI: 10.1038/s41419-020-03210-5
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WDHD1 is essential for the survival of PTEN-inactive triple-negative breast cancer

Abstract: Triple-negative breast cancer (TNBC) is the most aggressive type of breast cancer that lacks the oestrogen receptor, progesterone receptor and human epidermal growth factor receptor 2, making it difficult to target therapeutically. Targeting synthetic lethality is an alternative approach for cancer treatment. TNBC shows frequent loss of phosphatase and tensin homologue (PTEN) expression, which is associated with poor prognosis and treatment response. To identify PTEN synthetic lethal interactions, TCGA analysi… Show more

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Cited by 20 publications
(19 citation statements)
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“…Sources of cell lines and culture conditions were reported earlier ( Wang et al., 2014 ; Liu et al., 2019 ; Ertay et al., 2020 ). Details are provided in the Supplementary Methods .…”
Section: Methodsmentioning
confidence: 99%
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“…Sources of cell lines and culture conditions were reported earlier ( Wang et al., 2014 ; Liu et al., 2019 ; Ertay et al., 2020 ). Details are provided in the Supplementary Methods .…”
Section: Methodsmentioning
confidence: 99%
“…Mammosphere assay and quantifications were performed as previously described ( Ertay et al., 2020 ). Details are provided in the Supplementary Methods .…”
Section: Methodsmentioning
confidence: 99%
See 1 more Smart Citation
“…WDHD1 has also been reported to facilitate the abrogation of G1 checkpoint upon DNA damage, leading to genomic instability and eventually tumorigenesis ( Zhou et al, 2020 ). Moreover, WDHD1 could accelerate cell proliferation, cell viability, and metastasis in several cancers including cholangiocarcinoma and breast cancer ( Sato et al, 2010 ; Liu et al, 2019 ; Ertay et al, 2020 ; Zhou and Chen, 2021 ). In accordance with the above research, both our overall and disease free survival analysis exhibited that high levels of WDHD1 correlated with poor patient outcome ( Figures 4B , 5B ), confirming the oncogenic function of WDHD1 in pancreatic adenocarcinoma and expanding it roles in cancer biology which need further validations.…”
Section: Resultsmentioning
confidence: 99%
“…Among patients receiving neoadjuvant regimens containing docetaxel, carboplatin, trastuzumab and lapatinib, those with tumors with PIK3CA/ERBB family mutations seem to develop pathologic complete response (pCR) more than those with wild-type tumors [ 55 ]. For TNBC, the most common abnormal mechanism of PAM is PTEN inactivation or downregulation, accounting for 67% of cases [ 56 , 57 ]. In addition, mTOR hyperphosphorylation is associated with poor outcomes of patients with stage I/II TNBC [ 46 ].…”
Section: Changes Of the Pam Pathway In Different Breast Cancer Subtypesmentioning
confidence: 99%