Exogenous p27KIP1 expression induces anti-tumour effects and inhibits the EGFR/PI3K/Akt signalling pathway in PC3 cells

Xia, Dan; Luo, Jindan; Wang, Ping

doi:10.1038/aja.2009.51

Cited by 11 publications

(11 citation statements)

References 34 publications

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“…We also found that the decreased Akt activity corresponds to the enhanced expression of the proapoptotic protein Bad. This is consistent with the results of the studies by Jun et al [ 56 ]. Additionally, studies by Al-Bazz et al found a significant correlation between the expressions of Akt and Bad [ 57 ].…”

Section: Discussionsupporting

confidence: 94%

In Vivo Study of the Effects of ERβ on Apoptosis and Proliferation of Hormone-Independent Prostate Cancer Cell Lines PC-3M

Zhou

Guo

et al. 2018

BioMed Research International

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Objective To evaluate the in vivo therapeutic effects of attenuated Salmonella carrying PCDNA3.1-ERβ plasmid in hormone-independent prostatic cancer in nude mice and to clarify the mechanism by which estrogen receptor β (ERβ) induces apoptosis and proliferation in prostatic cancer cells in mice. Methods The orthotopic prostatic cancer models of mice were randomly divided as follows: MOCK group, treated with PBS, PQ group, treated with attenuated Salmonella alone, PQ-PCDNA3.1 group, treated with attenuated Salmonella carrying PCDNA3.1 plasmid, and PQ-PCDNA3.1-ERβ group, treated with the attenuated Salmonella carrying PCDNA3.1-ERβ plasmid. Then, 10 μl of the plasmid-containing solution, comprising 1 × 107 cfu of the bacteria, was administered via intranasal delivery to each group except the MOCK group. The experimental methods included flow cytometry and terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labelling (TUNEL) assay, immunohistochemistry, and western blotting. Results Compared with the MOCK, PQ, and PQ-PCDNA3.1 groups, the weights of tumors in the PQ-PCDNA3.1-ERβ group were significantly reduced. The results of flow cytometry and TUNEL assay revealed that the number of apoptotic cells in the PQ-PCDNA3.1-ERβ group significantly increased. Compared with PQ-PCDNA3.1 group, the protein expression levels of ERβ, Bad, p-caspase 9, p-caspase 3, and cleaved PARP in the PQ-PCDNA3.1-ERβ group were significantly increased, while the expression levels of Akt, p-Akt, and Bcl-xl were decreased (P < 0.05). Conclusion The attenuated Salmonella carrying PCDNA3.1-ERβ plasmid could inhibit the growth of orthotopic prostatic cancer in mice by increasing the expression of ERβ.

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Section: Discussionsupporting

confidence: 94%

In Vivo Study of the Effects of ERβ on Apoptosis and Proliferation of Hormone-Independent Prostate Cancer Cell Lines PC-3M

Zhou

Guo

et al. 2018

BioMed Research International

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“…Avoiding apoptosis is a hallmark of cancer, and downregulation of p27 is one mechanism by which tumor cells can achieve this goal (48,49,(56)(57)(58). Consistent with this, low levels of p27 are associated with poor prognosis in a number of human cancers, including breast cancer (38,40,48,55).…”

Section: Introductionmentioning

confidence: 59%

Hunk is required for HER2/neu-induced mammary tumorigenesis

Yeh¹,

Yang²,

Jung³

et al. 2011

J. Clin. Invest.

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Understanding the molecular pathways that contribute to the aggressive behavior of human cancers is a critical research priority. The SNF1/AMPK-related protein kinase Hunk is overexpressed in aggressive subsets of human breast, ovarian, and colon cancers. Analysis of Hunk -/-mice revealed that this kinase is required for metastasis of c-myc-induced mammary tumors but not c-myc-induced primary tumor formation. Similar to c-myc, amplification of the proto-oncogene HER2/neu occurs in 10%-30% of breast cancers and is associated with aggressive tumor behavior. By crossing Hunk -/-mice with transgenic mouse models for HER2/neu-induced mammary tumorigenesis, we report that Hunk is required for primary tumor formation induced by HER2/ neu. Knockdown and reconstitution experiments in mouse and human breast cancer cell lines demonstrated that Hunk is required for maintenance of the tumorigenic phenotype in HER2/neu-transformed cells. This requirement is kinase dependent and resulted from the ability of Hunk to suppress apoptosis in association with downregulation of the tumor suppressor p27 kip1 . Additionally, we find that Hunk is rapidly upregulated following HER2/neu activation in vivo and in vitro. These findings provide what we believe is the first evidence for a role for Hunk in primary tumorigenesis and cell survival and identify this kinase as an essential effector of the HER2/neu oncogenic pathway.

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“…Specifically, Zhang et al determined the knockdown of linc00152 can inhibit the cell cycle (especially the G1 phase) to delay cell proliferation. This was revealed by the considerable decrease in EGFR, PI3K, and AKT activities and the epithelial intercellular transition via the suppression of fibronectin and vimentin downstream of the EGFR/PI3K/AKT signaling pathway to inhibit cell invasion and migration, in addition to an increase in P21 production to promote apoptosis . This not only clarified the linc00152 mechanism related to the progression of NSCLC but also suggests that linc00152 is a potential therapeutic target.…”

Section: Molecular Functions and Mechanisms Of Linc00152 In Human Tumorsmentioning

confidence: 86%

Improved characterization of the relationship between long intergenic non‐coding RNA Linc00152 and the occurrence and development of malignancies

Guo

Jiang

et al. 2019

Cancer Medicine

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Linc00152, located on chromosome 2p11.2, is a long intergenic non‐coding RNA molecule with 828 nucleotides that is highly expressed in many types of human tumor tissues, especially in malignant tumors of the digestive system. Linc00152 promotes the occurrence and development of tumors by increasing tumor cell proliferation, invasion, metastasis, and apoptosis. Additionally, linc00152 contributes to the carcinogenesis of several cancers, including gastric cancer, liver cancer, hepatocellular carcinoma, gallbladder cancer, clear cell renal cell carcinoma, and colorectal cancer, by disturbing various signaling pathways (eg PI3K/AKT, mTOR, IL‐1, and NOTCH 1 signaling pathways). High linc00152 expression levels are associated with chemoresistance as well as poor prognosis and shorter survival. Continual advances made in the relevant research have indicated that linc00152 may be useful as a new tumor molecular biomarker, applicable for tumor diagnosis, targeted therapy, and prognosis assessment. This review summarizes the progress in the research into the relationship between linc00152 and the occurrence and development of malignancies based on molecular functions, regulatory mechanisms, and clinical applications.

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Exogenous p27KIP1 expression induces anti-tumour effects and inhibits the EGFR/PI3K/Akt signalling pathway in PC3 cells

Cited by 11 publications

References 34 publications

In Vivo Study of the Effects of ERβ on Apoptosis and Proliferation of Hormone-Independent Prostate Cancer Cell Lines PC-3M

In Vivo Study of the Effects of ERβ on Apoptosis and Proliferation of Hormone-Independent Prostate Cancer Cell Lines PC-3M

Hunk is required for HER2/neu-induced mammary tumorigenesis

Improved characterization of the relationship between long intergenic non‐coding RNA Linc00152 and the occurrence and development of malignancies

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