Proline rich 11 (PRR11) overexpression amplifies PI3K signaling and promotes antiestrogen resistance in breast cancer

Lee, Kyung-min; Guerrero-Zotano, Angel L.; Servetto, Alberto; Sudhan, Dhivya R.; Lin, Chang‐Ching; Formisano, Luigi; Jansen, Valerie M.; González-Ericsson, Paula I.; Sanders, Melinda E.; Stricker, Thomas; Raj, Ganesh V.; Dean, Kevin M.; Fiolka, Reto; Cantley, Lewis C.; Hanker, Ariella B.; Arteaga, Carlos L.

doi:10.1038/s41467-020-19291-x

Cited by 35 publications

(51 citation statements)

References 59 publications

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“…Interestingly, a similar result from cell cycle evaluation was observed in our research. Besides, cancer drug resistance also positively correlates with PRR11 expression level according to Lee et al's research [ 16 ], which may cause patients' poor prognosis. PRR11 has been proven to hold prognostic values and take a role as a carcinogenic factor in BC [ 17 ] (our bioinformatics prediction showed that patients with high expression of PRR11 suffered poor prognosis).…”

Section: Discussionmentioning

confidence: 99%

miR-204-5p Hampers Breast Cancer Malignancy and Affects the Cell Cycle by Targeting PRR11

Shen

et al. 2022

Computational and Mathematical Methods in Medicine

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Purpose. To unravel mechanisms of miR-204-5p in breast cancer (BC) cells. Methods. miR-204-5p expression level in BC cell lines was measured by qRT-PCR. Putative binding sites of miR-204-5p on the 3 ′ -untranslated region of PRR11 were predicted by the bioinformatics method and verified by the dual-luciferase method. Protein and mRNA levels of PRR11 in BC were determined by western blot and qRT-PCR. The association between two genes was analyzed by correlation analysis. Cancer cell functions were evaluated through CCK8, flow cytometry, and Transwell approaches. Results. Significant downregulation of miR-204-5p was observed in BC tissue and cells. Cell functional experiments showed the inhibition of miR-204-5p on cell behaviors and cell cycle. PRR11 was the downstream target of miR-204-5p. Inhibition of RPP11 could reverse the impacts of the miR-204-5p inhibitor on cell functions of BC. Conclusion. Our study revealed that the miR-204-5p/PRPP11 axis suppressed BC progression, which may provide a novel insight into the regulatory roles of miR-204-5p.

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Section: Discussionmentioning

confidence: 99%

miR-204-5p Hampers Breast Cancer Malignancy and Affects the Cell Cycle by Targeting PRR11

Shen

et al. 2022

Computational and Mathematical Methods in Medicine

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“…As application of subcutaneous model has advantage in monitoring the growth of tumor, tumor growth curve detection and evaluation of drug efficacy ( Masuelli et al, 2017 ; Ireson et al, 2019 ; Lee et al, 2020 ), we chose subcutaneous model to evaluate the inhibition effect by knocking down C1QBP or shC1QBP combined with PTX treatment. For the subcutaneously injected group, the volumes of tumors formed by the control cells were significantly greater than those from cells expressing lower levels of C1QBP ( Figure 3C ), suggesting that silencing C1QBP restrained cell proliferation in mice.…”

Section: Resultsmentioning

confidence: 99%

Hypoxia-Mediated Complement 1q Binding Protein Regulates Metastasis and Chemoresistance in Triple-Negative Breast Cancer and Modulates the PKC-NF-κB-VCAM-1 Signaling Pathway

Wu¹,

Chu²,

Sun³

et al. 2021

Front. Cell Dev. Biol.

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Graphical AbstractIn TNBC cells, the inhibition of C1QBP suppresses PKC–NF-κB signaling in cytoplasm, upregulating Iκβα expression, thereby decreasing the VCAM-1 expression by lowering p65 level in nucleus in normoxic conditions. When TNBC cells are exposed to hypoxic conditions, HIF-1α upregulates C1QBP expression. The inhibition of C1QBP notably suppresses the activation of hypoxia-induced PKC–NF-κB signaling and decreases VCAM-1 level, resulting in metastasis blocking and PTX drug chemoresistance decreasing of TNBC cells.

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“…The expression of PRR11 is closely related to tumorigenesis, progression and poor prognosis in cancers, including lung, gastric, pancreatic, breast, esophageal and ovarian cancers [15,[29][30][31][32][33]. PRR11 was also demonstrated to promote anti-estrogen resistance in breast cancer by amplifying the PI3K signaling pathway [34]. Additionally, PRR11 activated the Akt/mTOR autophagy signaling pathway to facilitate tumorigenesis in non-small cell lung cancer, suggesting that this gene may affect cancer cells through different signal transduction pathways.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-26b-5p suppresses the proliferation of tongue squamous cell carcinoma via targeting proline rich 11 (PRR11)

Liu

et al. 2021

Bioengineered

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MicroRNAs (miRNAs) have been proved to be involved in many biological processes during tumorigenesis and progression, including cell proliferation and cell cycle progression. However, the potential role of miR-26b-5p in tongue squamous cell carcinoma (TSCC) remains unclear. In the present study, we demonstrated that miR-26b-5p was decreased in TSCC tissues in both TCGA-TSCC subset and eight paired samples from TSCC patients, while Proline Rich 11 (PRR11) was obviously increased. Transfection of miR-26b-5p mimics inhibited CALL7 cell proliferation by arresting the cells at the S/G2 transition. Meanwhile, miR-26b-5p inhibitor had the opposite biological functions. The results of luciferase activity and RNA-pulldown assays indicated that miR-26b-5p directly targeted the PRR11 3 -untranslated region in CAL27 cells. Furthermore, the effects of miR-26b-5p on cell cycle regulation were reversed after treatment with siRNA against PRR11. In summary, our findings indicate that miR-26b-5p induce cell cycle arrest in TSCC by targeting PRR11. Hence, targeting miR-26b-5p could be a promising therapeutic strategy for the treatment of TSCC.

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Proline rich 11 (PRR11) overexpression amplifies PI3K signaling and promotes antiestrogen resistance in breast cancer

Cited by 35 publications

References 59 publications

miR-204-5p Hampers Breast Cancer Malignancy and Affects the Cell Cycle by Targeting PRR11

miR-204-5p Hampers Breast Cancer Malignancy and Affects the Cell Cycle by Targeting PRR11

Hypoxia-Mediated Complement 1q Binding Protein Regulates Metastasis and Chemoresistance in Triple-Negative Breast Cancer and Modulates the PKC-NF-κB-VCAM-1 Signaling Pathway

MicroRNA-26b-5p suppresses the proliferation of tongue squamous cell carcinoma via targeting proline rich 11 (PRR11)

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