Lipogenic gene expression profile in patients with gastric cancer

Miyachi, Kazuhito; Sawada, Y; Shida, Yohei; Sugawara, Akira; Higuchi, Hisashi

doi:10.3892/mco.2013.148

Cited by 9 publications

(7 citation statements)

References 20 publications

(19 reference statements)

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“…For example, Lv et al reported that the deletion, amplification or mutation at the precursor miR-33b was detected in 10% of medulloblastomas (23). Moreover, miR-33b and carnitine O-palmitoyltransferase type I were found to be significantly downregulated in gastric carcinoma, suggesting that the downregulation of miR-33b may be mediated by conditions that also affect the expression of lipogenic gene-related transcription factors (24). miR-33b has also been shown to be downregulated in multiple myeloma, and to be associated with disease progression and poor prognosis (25,26).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-33b suppresses the proliferation and metastasis of hepatocellular carcinoma cells through the inhibition of Sal-like protein 4 expression

Tian

Xiao

et al. 2016

International Journal of Molecular Medicine

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MicroRNAs (miRNAs or miRs) have been found to participate in the development and malignant progression of human cancers by negatively mediating the expression of their target genes. Recently, miR‑33b has been reported to be involved in multiple types of human cancer, including hepatocellular carcinoma (HCC). However, the underlying regulatory mechanisms of miR‑33b in HCC cell growth and metastasis remain largely unclear. In the present study, RT-qPCR revealed that miR‑33b was significantly downregulated in HCC tissues compared to their matched adjacent normal tissues. Moreover, the miR‑33b level was significantly lower in advanced-stage HCC (stages T3-T4) compared to early-stage HCC (stages T1-T2). Furthermore, it was also downregulated in the HCC cell lines, LH86, HepG2, LMH and PLHC-1, when compared with the THLE-3 normal human liver cells. We further demonstrated that the overexpression of miR‑33b led to a significant decrease in the proliferation, migration and invasion of HepG2 and LH86 cells. Luciferase reporter assay identified Sal-like protein 4 (SALL4) as a target gene of miR‑33b, and its protein expression was negatively regulated by miR‑33b in HepG2 and LH86 cells. Moreover, the restoration of SALL4 expression markedly reversed the inhibitory effect of miR‑33b overexpression on the proliferation, migration and invasion of HepG2 and LH86 cells, indicating that SALL4 is involved in miR‑33b-mediated malignant phenotypes of HCC cells. Furthermore, we found that SALL4 was significantly upregulated in HCC tissues compared to their matched adjacent normal tissues, and its increased expression was significantly associated with the advanced malignancy of HCC. Moreover, SALL4 was also upregulated in HCC cell lines compared to the THLE-3 normal human liver cells. Finally, we found that the SALL4 expression inversely correlated with the miR‑33b level in HCC tissues. On the whole, the findings of our study demonstrate that miR‑33b suppresses the proliferation and metastasis of HCC cells through the inhibition of SALL4 expression. Therefore, miR‑33b/SALL4 may become a potential therapeutic target for the treatment of HCC.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-33b suppresses the proliferation and metastasis of hepatocellular carcinoma cells through the inhibition of Sal-like protein 4 expression

Tian

Xiao

et al. 2016

International Journal of Molecular Medicine

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“…Numerous types of cancer exhibit increased de novo lipogenesis irrespective of the extracellular lipid availability ( 20 ). Exacerbated lipogenesis has been demonstrated to be one of main characteristics of cancer ( 19 ). The maintenance of intracellular lipid homeostasis depends on the balance between lipid biosynthesis and degradation ( 21 ).…”

Section: Discussionmentioning

confidence: 99%

“…Overexpression of SREBP-1 has been observed in atypically hyperplastic endometrium and endometrial cancer tissues, while knockdown of SREBP-1 dramatically inhibited the proliferating potential of endometrial cancer cells ( 17 ). The expression level of SREBP-1 is also elevated in certain types of tumors such as prostate and gastric cancer ( 18 , 19 ). However, the expression and function of SREBP-1 in human breast cancer remains to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

SREBP-1 is an independent prognostic marker and promotes invasion and migration in breast cancer

et al. 2016

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Re-programming of lipogenic signaling has been previously demonstrated to result in significant alterations in tumor cell pathology. Sterol regulatory element-binding protein 1 (SREBP-1) is a known transcription factor of lipogenic genes. Despite the fact that its functions in proliferation and apoptosis have been elucidated in recent studies, its role in tumor cell migration and invasion, particularly in breast cancer, remains unclear. In present study, the messenger RNA and protein expression levels of SREBP-1 in cancer tissues were observed to be overexpressed compared with those in matched para-cancerous tissues (P<0.01). SREBP-1 level was highly positively correlated with tumor differentiation (P<0.001), tumor-node-metastasis stage (P=0.044) and lymph node metastasis (P<0.001). High expression of SREBP-1 predicted poor prognosis in patients with breast cancer. Additionally, multivariate analysis revealed that SREBP-1 was an independent factor of 5-year overall and disease-specific survival in breast cancer patients (P<0.01). In vitro studies revealed that the suppression of SREBP-1 expression in both MDA-MB-231 and MCF7 cells significantly inhibited cell migration and invasion (P<0.01). The present data indicate that SREBP-1 plays a critical role in breast cancer migration and invasion, and may serve as a prognostic marker of this malignancy.

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“…In bladder cancer, SREBP-1 promotes tumor growth via regulating the expression of key lipogenic enzymes [10]. This phenomenon was also observed in endometrial cancer, prostate cancer and gastric cancer [11–13]. Despite the few studies that have shown that SREBP-1 could enhance lipid synthesis in HCC cells, the clinical significance of SREBP-1 in HCC and its role in tumor progression are still poorly understood.…”

Section: Introductionmentioning

confidence: 99%

“…A recent study found that silencing of SREBP-1 led to significant changes in carbohydrate metabolism via upregulation of gluconeogenesis gene expression, and decreased glycolysis and glycogen synthesis gene expression in an animal model of obesity and type 2 diabetes [ 8 ]. Additionally, SREBEP-1 overexpression has been reported in various human cancers and its abnormal expression is associated with malignant characteristics [ 9 – 13 ]. SREBP-1 was significantly higher in ovarian cancer compared with benign and borderline ovarian tumors.…”

Section: Introductionmentioning

confidence: 99%

SREBP-1 Has a Prognostic Role and Contributes to Invasion and Metastasis in Human Hepatocellular Carcinoma

Yang

Zhang

et al. 2014

IJMS

102

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Sterol regulatory element-binding protein 1 (SREBP-1) is a well-known nuclear transcription factor involved in lipid synthesis. Recent studies have focused on its functions in tumor cell proliferation and apoptosis, but its role in cell migration and invasion, especially in hepatocellular carcinoma (HCC), is still unclear. In this study, we found that the expression of SREBP-1 in HCC tissues was significantly higher than those in matched tumor-adjacent tissues (p < 0.05). SREBP-1 was expressed at significantly higher levels in patients with large tumor size, high histological grade and advanced tumor-node-metastasis (TNM) stage (p < 0.05). The positive expression of SREBP-1 correlated with a worse 3-year overall and disease-free survival of HCC patients (p < 0.05). Additionally, SREBP-1 was an independent factor for predicting both 3-year overall and disease-free survival of HCC patients (p < 0.05). In vitro studies revealed that downregulation of SREBP-1 inhibited cell proliferation and induced apoptosis in both HepG2 and MHCC97L cells (p < 0.05). Furthermore, wound healing and transwell assays showed that SREBP-1 knockdown prominently inhibited cell migration and invasion in both HepG2 and MHCC97L cells (p < 0.05). These results suggest that SREBP-1 may serve as a prognostic marker in HCC and may promote tumor progression by promoting cell growth and metastasis.

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Lipogenic gene expression profile in patients with gastric cancer

Cited by 9 publications

References 20 publications

MicroRNA-33b suppresses the proliferation and metastasis of hepatocellular carcinoma cells through the inhibition of Sal-like protein 4 expression

MicroRNA-33b suppresses the proliferation and metastasis of hepatocellular carcinoma cells through the inhibition of Sal-like protein 4 expression

SREBP-1 is an independent prognostic marker and promotes invasion and migration in breast cancer

SREBP-1 Has a Prognostic Role and Contributes to Invasion and Metastasis in Human Hepatocellular Carcinoma

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