STAMBPL1 promotes breast cancer cell resistance to cisplatin partially by stabilizing MKP-1 expression

Liu, Rong; Yang, Guangxi; Bao, Min; Zhou, Zhongmei; Mao, Xiaoyun; Liu, Wenjing; Jiang, Xingming; Zhu, Di; Ren, Xinle; Huang, Jian; Chen, Ceshi

doi:10.1038/s41388-022-02252-7

Cited by 11 publications

(6 citation statements)

References 42 publications

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“…Western blotting was performed to detect the knockdown effect of STAMBPL1 protein in animal experiments (Figure S1A). We observed that depletion of STAMBPL1 signi cantly suppressed breast cancer cell growth in vivo, which is consistent with our previous report [14] . STAMBPL1 signi cantly inhibited the tumor growth based on the tumor volume and the tumor weight (Fig.…”

Section: Stambpl1 Promotes Tnbc Angiogenesissupporting

confidence: 93%

“…Targeting STAMBPL1 has been shown to promote the degradation of XIAP and trigger apoptosis in prostate cancer cells, suggesting that STAMBPL1 may be a potential therapeutic target for prostate cancer [13] . Our previous studies have con rmed that STAMBPL1 promotes cisplatin resistance in TNBC cells by deubiquitinating and stabilizing phosphatase MKP-1 expression [14] . However, the roles and mechanisms of STAMBPL1 in breast cancer angiogenesis have not been investigated.…”

Section: Introductionmentioning

confidence: 92%

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STAMBPL1 promotes triple-negative breast cancer angiogenesis by upregulating the transcription of GRHL3/HIF1α/VEGFA via FOXO1

Chen,

Fang,

Liang

et al. 2024

Preprint

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Anti-angiogenesis is a crucial therapeutic strategy for triple-negative breast cancer (TNBC), but the current targeted drugs are insufficient to meet clinical requirements. Our study has discovered that silencing the deubiquitinating enzyme STAMBPL1 can effectively inhibit the growth and angiogenesis of TNBC xenografts in nude mice. STAMBPL1 promotes the expression of HIF1α/VEGFA in TNBC through a non-enzymatic-dependent mechanism. STAMBPL1 interacts with the transcription factor FOXO1, which binds to the promoter of the GRHL3 gene, thereby positively regulating its transcription. Subsequently, GRHL3 binds to the HIF1α gene promoter to promote its transcription and angiogenesis. Moreover, we have demonstrated that the combination of FOXO1 inhibitor AS1842856 and VEGFR inhibitor Apatinib significantly inhibited the growth of transplanted tumors in nude mice. These findings indicate that the STAMBPL1/FOXO1/GRHL3/HIF1α/VEGFA axis provides potential therapeutic targets in TNBC.

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Section: Stambpl1 Promotes Tnbc Angiogenesissupporting

confidence: 93%

Section: Introductionmentioning

confidence: 92%

STAMBPL1 promotes triple-negative breast cancer angiogenesis by upregulating the transcription of GRHL3/HIF1α/VEGFA via FOXO1

Chen,

Fang,

Liang

et al. 2024

Preprint

Self Cite

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“…Recent study have demonstrated that inhibition of JNK and PARP1 can reverse miRNA-363-3p-associated doxorubicin resistance in diffuse large B-cell lymphoma [ 43 ]. Depleting STAMBPL1 and MKP-1 can enhance the sensitivity of breast cancer cells to cisplatin by increasing JNK phosphorylation and activation [ 44 ]. In addition, upregulation of Tiam1 expression could also promote radioresistance in laryngeal squamous cell carcinoma by activating the JNK/ATF-2 signaling [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

TRAF4-mediated ubiquitination-dependent activation of JNK/Bcl-xL drives radioresistance

Dong

Gan

et al. 2023

Cell Death Dis

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The E3 ligase TNF receptor-associated factor 4 (TRAF4) is upregulated and closely associated with tumorigenesis and the progression of multiple human malignancies. However, its effect on radiosensitivity in colorectal cancer (CRC) has not been elucidated. The present study found that TRAF4 was significantly increased in CRC clinical tumor samples. Depletion of TRAF4 impaired the malignant phenotype of CRC cells and sensitized irradiation-induced cell death. Irradiation activated the c-Jun N-terminal kinases (JNKs)/c-Jun signaling via increasing JNKs K63-linked ubiquitination and phosphorylation. Furthermore, c-Jun activation triggered the transcription of the antiapoptotic protein Bcl-xL, thus contributing to the radioresistance of CRC cells. TRAF4 was positively correlated with c-Jun and Bcl-xL, and blocking TRAF4 or inhibiting Bcl-xL with inhibitor markedly promoted ionizing radiation (IR)-induced intrinsic apoptosis and sensitized CRC cells to radiotherapy in vitro and in vivo. Our findings illustrate a potential mechanism of radioresistance, emphasizing the clinical value of targeting the TRAF4/Bcl-xL axis in CRC therapy.

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“…Our results corroborate the findings that BIRC3 functions as a tumor suppressor. The study by Liu et al (2022) found that STAMBPL1 interacts with MKP-1 and stabilizes MKP-1 via deubiquitination, further promoting breast cancer cell resistance to cisplatin. Moreover, STAMBPL1 could regulate snail stability by deubiquitination mechanisms in breast cancer (Ambroise et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Identification of ubiquitination-related gene classification and a novel ubiquitination-related gene signature for patients with triple-negative breast cancer

Zhao

Zheng

et al. 2023

Front. Genet.

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Background: Ubiquitination-related genes (URGs) are important biomarkers and therapeutic targets in cancer. However, URG prognostic prediction models have not been established in triple-negative breast cancer (TNBC) before. Our study aimed to explore the roles of URGs in TNBC.Methods: The Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) and the Gene Expression Omnibus (GEO) databases were used to identify URG expression patterns in TNBC. Non-negative matrix factorization (NMF) analysis was used to cluster TNBC patients. The least absolute shrinkage and selection operator (LASSO) analysis was used to construct the multi-URG signature in the training set (METABRIC). Next, we evaluated and validated the signature in the test set (GSE58812). Finally, we evaluated the immune-related characteristics to explore the mechanism.Results: We identified four clusters with significantly different immune signatures in TNBC based on URGs. Then, we developed an 11-URG signature with good performance for patients with TNBC. According to the 11-URG signature, TNBC patients can be classified into a high-risk group and a low-risk group with significantly different overall survival. The predictive ability of this 11-URG signature was favorable in the test set. Moreover, we constructed a nomogram comprising the risk score and clinicopathological characteristics with favorable predictive ability. All of the immune cells and immune-related pathways were higher in the low-risk group than in the high-risk group.Conclusion: Our study indicated URGs might interact with the immune phenotype to influence the development of TNBC, which contributes to a further understanding of molecular mechanisms and the development of novel therapeutic targets for TNBC.

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STAMBPL1 promotes breast cancer cell resistance to cisplatin partially by stabilizing MKP-1 expression

Cited by 11 publications

References 42 publications

STAMBPL1 promotes triple-negative breast cancer angiogenesis by upregulating the transcription of GRHL3/HIF1α/VEGFA via FOXO1

STAMBPL1 promotes triple-negative breast cancer angiogenesis by upregulating the transcription of GRHL3/HIF1α/VEGFA via FOXO1

TRAF4-mediated ubiquitination-dependent activation of JNK/Bcl-xL drives radioresistance

Identification of ubiquitination-related gene classification and a novel ubiquitination-related gene signature for patients with triple-negative breast cancer

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