Overexpression of SMYD3 and matrix metalloproteinase-9 are associated with poor prognosis of patients with gastric cancer

Liu, Yong; Liu, Honggen; Luo, Xue‐Gang; Deng, Jingyu; Pan, Yuan; Liang, Han

doi:10.1007/s13277-015-3077-z

Cited by 44 publications

(29 citation statements)

References 26 publications

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“…MMPs are critical players in tumor migration and invasion through degradation of ECM components. Other studies have shown that MMP-2 expression is significantly relevant for the tumor metastasis (35) and expression of MMP-9 is closely related to poor prognosis and metastasis of CRC (36). MMP-2 and MMP-9 are frequently upregulated in cancer cells (37,38).…”

Section: Discussionmentioning

confidence: 96%

miR-27a promotes proliferation, migration, and invasion of colorectal cancer by targeting FAM172A and acts as a diagnostic and prognostic biomarker

et al. 2017

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Accumulating evidence shows that mircroRNAs (miRNAs) play a crucial role in the development of colorectal cancer. In our previous study, FAM172A was demonstrated to be a novel tumor suppressor gene in CRC. Therefore, the aim of the present study was to identify whether the miR‑27a could be a diagnostic and prognostic marker and the regulatory relationships between miR‑27a and FAM172A. We demonstrated high levels of miR‑27a expression in tissues of patients with CRC as well as in CRC cell lines. There was a positive correlation between the levels of miR‑27a and the poor overall survival of patients with CRC. Furthermore, elevated levels of miR‑27a expression were associated with TNM stage and distant metastasis. Increased expression or inhibition of miR‑27a promoted or inhibited the metastasis of CRC cell lines, respectively. Moreover, we showed that miR‑27a directly targets the 3'-untranslated region of FAM172A mRNA by using a dual-luciferase assay. Increased or decreased expression of FAM172A expression was observed when miR‑27a expression was inhibited or elevated in the CRC cells, respectively. In summary, our study showed that miR‑27a expression is a diagnostic and prognostic marker and correlates with overall survival of patients with CRC. Therefore, it may be a therapeutic approach for preventing metastasis of CRC to inhibit expression of miR‑27a or increase expression of FAM172A.

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Section: Discussionmentioning

confidence: 96%

miR-27a promotes proliferation, migration, and invasion of colorectal cancer by targeting FAM172A and acts as a diagnostic and prognostic biomarker

et al. 2017

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“…For instance, the liver and breast human cancer sample dataset from the "The Cancer Genome Atlas" (TCGA) revealed that SMYD3 transcript levels correlate with expression of key proliferation [18] and EMT genes [18,35]. In addition, SMYD3 expression was positively associated, respectively, with the metalloproteinases MMP-2 and MMP-9 expression in pancreatic and gastric cancer tissues [92,93].…”

Section: Mouse Experimental Model Pancreatic Ductal and Lung Adenocarmentioning

confidence: 99%

SMYD3: An Oncogenic Driver Targeting Epigenetic Regulation and Signaling Pathways

Bottino

Peserico

Simone

et al. 2020

Cancers

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SMYD3 is a member of the SMYD lysine methylase family and plays an important role in the methylation of various histone and non-histone targets. Aberrant SMYD3 expression contributes to carcinogenesis and SMYD3 upregulation was proposed as a prognostic marker in various solid cancers. Here we summarize SMYD3-mediated regulatory mechanisms, which are implicated in the pathophysiology of cancer, as drivers of distinct oncogenic pathways. We describe SMYD3-dependent mechanisms affecting cancer progression, highlighting SMYD3 interplay with proteins and RNAs involved in the regulation of cancer cell proliferation, migration and invasion. We also address the effectiveness and mechanisms of action for the currently available SMYD3 inhibitors. The findings analyzed herein demonstrate that a complex network of SMYD3-mediated cytoplasmic and nuclear interactions promote oncogenesis across different cancer types. These evidences depict SMYD3 as a modulator of the transcriptional response and of key signaling pathways, orchestrating multiple oncogenic inputs and ultimately, promoting transcriptional reprogramming and tumor transformation. Further insights into the oncogenic role of SMYD3 and its targeting of different synergistic oncogenic signals may be beneficial for effective cancer treatment.

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“…Previous results have shown that SMYD3 is expressed differentially in normal and cancer tissues (21)(22)(23)(24). SMYD3 overexpression has been associated with progression in gastric and breast cancer (23,25). However, the effect of altered SMYD3 expression on the progression of glioma cells remains elusive.…”

Section: Discussionmentioning

confidence: 99%

SET and MYND domain-containing protein 3 is overexpressed in human glioma and contributes to tumorigenicity

et al. 2015

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SET and MYND domain-containing protein 3 (SMYD3) is a histone H3 lysine 4 (H3K4) di- and tri-methyltransferase that forms a transcriptional complex with RNA polymerase II and plays an important role in early embryonic lineage commitment through the activation of lineage-specific genes. SMYD3 activates the transcription of oncogenes and cell cycle genes in gastric and breast cancer cells. However, the contribution of SMYD3 in glioma tumorigenesis remains unknown. Here, we determined the expression of SMYD3 and assessed its clinical significance in human glioma. We found that SMYD3 was overexpressed in human glioma but not in normal brain tissue. The level of SMYD3 protein expression in human glioma tissues was directly correlated with the glioma grade. The level of SMYD3 protein expression in human glioma tissues was inversely correlated with patient survival. Enforced SMYD3 expression promoted glioma LN-18 cell proliferation. Inhibition of SMYD3 expression in glioma T98G cells suppressed their anchorage‑independent growth in vitro and tumorigenicity in vivo. Furthermore, we found that SMYD3 regulated the expression of p53 protein, which is essential in SMYD3‑induced cell growth in glioma cells. These results showed that SMYD3 is overexpressed in human glioma and contributes to glioma tumorigenicity through p53. Therefore, SMYD3 may be a new potential therapeutic target for human malignant glioma.

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Overexpression of SMYD3 and matrix metalloproteinase-9 are associated with poor prognosis of patients with gastric cancer

Cited by 44 publications

References 26 publications

miR-27a promotes proliferation, migration, and invasion of colorectal cancer by targeting FAM172A and acts as a diagnostic and prognostic biomarker

miR-27a promotes proliferation, migration, and invasion of colorectal cancer by targeting FAM172A and acts as a diagnostic and prognostic biomarker

SMYD3: An Oncogenic Driver Targeting Epigenetic Regulation and Signaling Pathways

SET and MYND domain-containing protein 3 is overexpressed in human glioma and contributes to tumorigenicity

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