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SIRT4 is upregulated in breast cancer and promotes the proliferation, migration and invasion of breast cancer cells.


ABSTRACT: BACKGROUND:Several members of the SIRT family (SIRT1-7), a highly conserved family of NAD+-dependent enzymes, play an important role in tumor formation. Recently, several studies have suggested that SIRT4 may function as both a tumor oncogene and a tumor suppressor. However, its relationship with breast cancer remains unclear. METHODS:We investigated SIRT4 protein levels in breast cancer and its possible association with selected clinicopathological parameters by immunohistochemical staining of a tissue microarray that included samples from 94 breast cancer patients. We further invested the effect of SIRT4 on the proliferation, migration and invasion of breast cancer cells. RESULTS:SIRT4 protein levels in breast were markedly higherthan their non-neoplastic tissue counterparts (P<0.001). Additionally, SIRT4 promoted the proliferation, migration and invasion of breast cancer cells. CONCLUSIONS:Our results show that SIRT4 possess oncogenic properties at the human cancer cell level and indicate that SIRT4 may participate in the development of breast cancer.

SUBMITTER: Huang G 

PROVIDER: S-EPMC6966060 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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SIRT4 is upregulated in breast cancer and promotes the proliferation, migration and invasion of breast cancer cells.

Huang Guoyu G   Lin Yao Y   Zhu Guanbao G  

International journal of clinical and experimental pathology 20171201 12


<h4>Background</h4>Several members of the SIRT family (SIRT1-7), a highly conserved family of NAD<sup>+</sup>-dependent enzymes, play an important role in tumor formation. Recently, several studies have suggested that SIRT4 may function as both a tumor oncogene and a tumor suppressor. However, its relationship with breast cancer remains unclear.<h4>Methods</h4>We investigated SIRT4 protein levels in breast cancer and its possible association with selected clinicopathological parameters by immuno  ...[more]

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