Increased expression of annexin A1 predicts poor prognosis in human hepatocellular carcinoma and enhances cell malignant phenotype

Lin, Yi-Ting; Lin, Guoqing; Fang, Wenzhen; Zhu, Hongwei; Chu, Kedan

doi:10.1007/s12032-014-0327-7

Cited by 42 publications

(37 citation statements)

References 23 publications

(27 reference statements)

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“…miR-26a regulated the proliferation and growth of cancer cells by targeting chromodomain helicase DNA binding protein 1 (35), growth regulation by estrogen in breast cancer 1 (35) and β-catenin (36). A number of studies demonstrated that the expression levels of miR-26a decreased in various types of tumor (23,37,38), whereas ANXA1 protein was overexpressed (39)(40)(41). Combined with the results of the present study suggesting that the miR-26a mimic may reduce the expression levels of ANXA1, a negative correlation was identified between miR-26a and ANXA1 in numerous tumors.…”

Section: Discussionsupporting

confidence: 78%

MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer

et al. 2018

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Abstract. The aim of the present study was to investigate the expression and role of microRNA-26a (miR-26a) in lung cancer, and to verify whether differentially expressed in adenocarcinoma of the lung (DAL-1) is the target protein of miR-26a. mRNA expression levels of miR-26a and DAL-1 were detected using reverse transcription-quantitative polymerase chain reaction. Protein expression levels of DAL-1 and annexin A1 (ANXA1) were evaluated by western blot analysis. Cell Counting Kit-8, Transwell and wound scratch healing assays were used to characterize the function of miR-26a in lung cancer cells. The association of DAL-1 with miR-26a or ANXA1 was determined by dual-luciferase reporter or two-dimensional gel electrophoresis assays. miR-26a revealed decreased expression levels in lung cancer tissues compared with normal lung tissues, and decreased expression levels in lung cancer cells compared with 16HBE cells. Inhibition of miR-26a promoted lung cancer cell growth, migration and invasion. The DAL-1 protein exhibited downregulated expression levels in lung cancer tissues. DAL-1 was not the direct target gene of miR-26a. The two-dimensional gel electrophoresis assay confirmed that DAL-1 and ANXA1 were associated proteins. Expression levels of the ANXA1 protein were increased following DAL-1 gene silencing. The altered expression level of miR-26a affected the expression of ANXA1, and not of DAL-1. miR-26a demonstrated decreased expression levels in lung cancer cells, and it has an important effect on the biological function of lung cancer cells. However, DAL-1 was not a target gene of miR-26a. As a DAL-1 associated protein, ANXA1 was regulated by miR-26a. IntroductionLung cancer has a high incidence of tumor recurrence and metastasis, and is the most common cause of cancer-associated morality worldwide (1). The overall 5-year survival rate among patients with lung cancer is <15%, and a high rate of metastasis is the primary cause of lung cancer-associated mortality (2). A previous study confirmed that differentially expressed in adenocarcinoma of the lung (DAL-1), a protein that belongs to the membrane-associated cytoskeleton protein 4.1 family, is an efficient suppressor of epithelial-mesenchymal transition (EMT) in lung cancer (3). EMT is a pivotal event in lung cancer metastasis progression (4-6). However, the regulators of DAL-1 in EMT remain unknown.Recently, a novel batch of endogenous small non-coding regulatory RNAs (microRNA's; miRNA's) have received attention in the development of cancer, miRNA's bind complementary sequences in target mRNAs, resulting in selective degradation or selective inhibition of their translation (7). The present study investigated the possible miRNAs of DAL-1 using bioinformatic assays, which included miR-26b, miR-26a, miR-96 and miR-223. Among them, the regulation of DAL-1 by miR-223 has been demonstrated to serve a role in gastric cancer (8). The present study revealed that the gene silencing of DAL-1 induced annexin A1 (ANXA1) protein expression levels to increase in H460 cells...

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Section: Discussionsupporting

confidence: 78%

MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer

et al. 2018

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“…Previous reports suggest that ANXA1 is involved in membrane aggregation, cell matrix interaction, vesicle transport, phagocytosis, proliferation, apoptosis, inflammation and cell transformation29. ANXA1 expression is up-regulated in breast cancer30, hepatocellular carcinoma31, melanoma32, and rectal cancer, but down regulated in nasopharyngeal carcinoma33 and cervical cancer34. In breast cancer, ANXA1 expression is associated with BRCA1/2 mutations35.…”

Section: Discussionmentioning

confidence: 99%

“…In breast cancer, ANXA1 expression is associated with BRCA1/2 mutations35. Similarly, high ANXA1 expression correlated with advanced TNM stage and poor survival of human hepatocellular carcinoma (HCC) patients31. It has been shown that ANXA1 expressing cancer cells are resistant to chemo- and radiation therapy because these cells acquired cancer stem cell like features3637.…”

Section: Discussionmentioning

confidence: 99%

Identification of specific biomarkers for gastric adenocarcinoma by ITRAQ proteomic approach

Wang

Zhi

Liu

et al. 2016

Sci Rep

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The aim of this study was to identify biomarkers for gastric cancer (GC) by iTRAQ. Using proteins extracted from a panel of 4 pairs of gastric adenocarcinoma samples (stage III-IV, Her-2 negative), we identified 10 up regulated and 9 down regulated proteins in all four pairs of GC samples compared to adjacent normal gastric tissue. The up regulated proteins are mainly involved in cell motility, while the down regulated proteins are mitochondrial enzymes involved in energy metabolism. The expression of three up regulated proteins (ANXA1, NNMT, fibulin-5) and one of the down regulated proteins (UQCRC1) was validated by Western Blot in 97 GC samples. ANXA1 was up regulated in 61.36% of stage I/II GC samples compared to matched adjacent normal gastric tissue, and its expression increased further in stage III/IV samples. Knockdown of ANXA1 by siRNA significantly inhibited GC cell migration and invasion, whereas over expression of ANXA1 promoted migration and invasion. We found decreased expression of UQCRC1 in all stages of GC samples. Our data suggest that increased cell motility and decreased mitochondrial energy metabolism are important hallmarks during the development of GC.

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“…Secondly, there are differences in the understanding of the roles of ANXA1 in tumorigenesis. In some tumors, ANXA1 has been shown to stimulate cell proliferation and promote the invasion and metastasis of tumors (14,21–24), whereas in other tumors, ANXA1 has been shown to exhibit the characteristics of a tumor suppressor gene, such as inhibiting cell proliferation and inducing apoptosis (11,25–28). Thus, the expression of ANXA1 in malignant tumors seems to be tumor-specific, and plays multi-factorial roles.…”

Section: Discussionmentioning

confidence: 99%

Effect of Annexin A1 gene on the proliferation and invasion of esophageal squamous cell carcinoma cells and its regulatory mechanisms

Han¹,

Lü²,

Huang³

et al. 2016

International Journal of Molecular Medicine

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The aim of this study was to examine the effect of Annexin A1 (ANXA1) on the proliferation, migration and invasion of esophageal squamous cell carcinoma (ESCC) cells and its possible mechanisms of action. After constructing the ANXA1 overexpression plasmid, we transfected this plasmid and/or microRNA (miRNA)-196a mimic into ESCC cells (Eca109 cell line). Methyl thiazolyl tetrazolium (MTT) assay and Transwell chamber assay were performed to determine cell proliferation, migration and invasion, respectively. Western blot analysis was used to examine the protein expression levels of ANXA1, Snail and E-cadherin. RT-PCR was used to detect the expression of miRNA-196a. Our results revealed that ANXA1 expression was upregulated in the cells transfected with the ANXA1 overexpression plasmid, and cell proliferation, migration and invasion were significantly increased (p=0.004, p<0.001 and p=0.011, respectively). In the cells transfected with the miRNA-196a mimic, miRNA-196a expression was significantly upregulated (p<0.001). However, miRNA-196a expression was downregulated in the cells transfected with the ANXA1 overexpression plasmid. In addition, in the cells transfected with the miRNA-196a mimic, cell proliferation, migration and invasion were significantly decreased (p=0.027, p=0.009 and p=0.021, respectively). In the cells transfected with the ANXA1 overexpression plasmid, the expression of Snail was upregulated and that of E-cadherin was downregulated. However, the opposite was observed in the cells transfected with the miRNA-196a mimic. Our findings thus demonstrate that ANXA1 promotes the proliferation of Eca109 cells, and increases the expression of Snail, whereas it inhibits that of E-cadherin, thus enhancing the migration and invasion of ESCC cells. miRNA-196a negatively regulates the expression of ANXA1, thereby inhibiting the proliferation, invasion and metastasis of ESCC cells.

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Increased expression of annexin A1 predicts poor prognosis in human hepatocellular carcinoma and enhances cell malignant phenotype

Cited by 42 publications

References 23 publications

MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer

MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer

Identification of specific biomarkers for gastric adenocarcinoma by ITRAQ proteomic approach

Effect of Annexin A1 gene on the proliferation and invasion of esophageal squamous cell carcinoma cells and its regulatory mechanisms

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