Decreased annexin A3 expression correlates with tumor progression in papillary thyroid cancer

Jung, Eun-Jung; Moon, Hyeong‐Gon; Park, Soon-Tae; Cho, Bok-Im; Lee, Sun Min; Jeong, Chi Young; Ju, Young‐Tae; Jeong, Sang‐Ho; Lee, Young-Joon; Choi, Sang-Kyung; Ha, Woo-Song; Lee, Jong Sil; Kang, Kee Ryeon; Hong, Soon Chan

doi:10.1002/prca.200900063

Cited by 31 publications

(25 citation statements)

References 24 publications

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“…It has been reported that Annexins, such as Annexin A1, A2 A3, A5 and A7, are closely associated with cancers [20]. In this study, we detected these five Annexins genes in CRC tissues.…”

Section: Resultsmentioning

confidence: 64%

The MiR-495/Annexin A3/P53 Axis Inhibits the Invasion and EMT of Colorectal Cancer Cells

Bai¹,

Wang²,

Wang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: More and more reports have shown that the dysregulation of miRNAs can contribute to the progression and metastasis of human cancers. Many studies have shown that the down-regulation of the miR-495 level occurs in a variety of cancers, including colorectal cancer (CRC). However, the precise molecular mechanisms of miR-495 in CRC have not been well clarified. In the current study, we investigated the biological functions and molecular mechanisms of miR-495 in CRC cell lines. Methods: qRT-PCR was used to determine the level of miR-495 in CRC cell lines and tissues. A miR-495 mimic and inhibitor were transfected into CRC cells, and the effects of miR-495 on the invasion and EMT were explored by qRT-PCR as well as transwell and Western blot assays. Meanwhile, luciferase assays were performed to validate Annexin A3 as a miR-495 target in CRC cells. Results: In our study, we found that miR-495 is down-regulated in CRC tissues and cell lines. Moreover, the low level of miR-495 was associated with increased expression of Annexin A3 in CRC tissues and cell lines. The invasion and EMT of CRC cells were suppressed by the overexpression of miR-495. However, the down-regulation of miR-495 promoted the invasion and EMT of CRC cells. Bioinformatics analysis predicted that Annexin A3 was a potential target gene of miR-495. Next, the luciferase reporter assay confirmed that miR-495 could directly target Annexin A3. Consistent with the effect of miR-495, the down-regulation of Annexin A3 by siRNA inhibited the invasion and EMT of CRC cells through the up-regulation of p53. The introduction of Annexin A3 in CRC cells partially blocked the effects of the miR-495 mimic. Conclusion: The introduction of miR-495 directly targeted Annexin A3 to inhibit the invasion and EMT of CRC cells by up-regulating p53, and the down-regulation of Annexin A3 was essential for inhibiting the invasion and EMT of CRC cells by overexpressing miR-495. Overall, the re-activation of the miR-495/Annexin A3/ p53 axis may represent a new strategy for overcoming metastasis of CRC.

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“…It has been reported that Annexins, such as Annexin A1, A2 A3, A5 and A7, are closely associated with cancers [20]. In this study, we detected these five Annexins genes in CRC tissues.…”

Section: Resultsmentioning

confidence: 64%

The MiR-495/Annexin A3/P53 Axis Inhibits the Invasion and EMT of Colorectal Cancer Cells

Bai¹,

Wang²,

Wang³

et al. 2017

Cell Physiol Biochem

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“…Although it has not been extensively studied in NPC cells, annexin A3 has prognostic relevance in prostate cancer (20), lung adenocarcinoma (21) and papillary thyroid cancer (22). Skvortsova et al (6) identified annexin A2 and A3 as novel biomarkers in prostate cancer cell lines using two-dimensional difference gel electrophoresis and matrix-assisted laser desorption ionization time-of-flight (TOF)/TOF-mass spectrometry; however, annexin A3 was not verified.…”

Section: Discussionmentioning

confidence: 99%

Protein expression of nucleophosmin, annexin A3 and nm23-H1 correlates with human nasopharyngeal carcinoma radioresistance in vivo

Liang

et al. 2016

Oncology Letters

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Abstract. Radioresistance is a significant obstacle in the treatment of endemic nasopharyngeal carcinoma (NPC). The present study aimed to identify proteins associated with radioresistance in NPC in vitro and in vivo. Proteomics analyses were conducted to screen for differentially-expressed proteins (DEPs) in parental CNE-2 cells and CNE-2R cells. Using proteomics approaches, 16 DEPs were identified. Of these DEPs, nucleophosmin (NPM1), annexin A3 and nm23-H1, were verified using western blot analyses. The tumorigenicity was investigated using mouse xenograft tumorigenicity assays, and tumor growth curves were generated. The protein expression of NPM1, annexin A3 and nm23-H1 was examined by immunohistochemically staining tumor tissues. NPM1 and annexin A3 protein levels were downregulated in the CNE-2R cells, whereas nm23-H1 expression was upregulated. In vivo tests showed that compared with the CNE-2 tumors, CNE-2R tumor growth was significantly retarded (P<0.05). CNE-2 tumor progression was inhibited by irradiation, but CNE-2R tumor progression was not, indicating that the CNE-2R cells were also radioresistant in vivo. NPM1 and annexin A3 expression was significantly lower in non-irradiated (NIR)-CNE-2R tumors compared with NIR-CNE-2 tumors (P<0.01). However, Nm23-H1 protein levels were significantly higher (P<0.05). Overall, the present study established comparable radioresistant and radiosensitive tumor models of human NPC, and identified candidate biomarkers that may correlate with radioresistance. The data showed that dysregulation of NPM1, annexin A3 and nm23-H1 expression correlated with the cellular and tumor radioresponse. These proteins are involved in the regulation of intracellular functions, including stress responses, cell proliferation and DNA repair. However, further clinical evaluations are required.

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“…It has three different domain composition: a short The C-terminus domain including four conserved ‘annexin repeat’ domains I, II, III and IV, a repeated collagen-like sequence, and a COOH-terminal domain including a single carbohydrate recognition-binding domain [14–15]. It is a membrane associated protein involved in the regulation of varieties of biological responses, containing cell proliferation, angiogenesis, cancer progression and metastasis [16–18]. ANXA3has been identified as a putative tumor oncogene in a diversity of carcinomas, such as Ovarian carcinoma, Lung adenocarcinoma, hepatocellular carcinoma, Colorectal cancer [19–22].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of ANXA3 is an independent prognostic indicator in gastric cancer and its depletion suppresses cell proliferation and tumor growth

Wang

2016

Oncotarget

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BackgroundGastric cancer (GC) is one of the most common malignancies worldwide. Tumour metastasis is one of the leading causes of death in GC patients. This study aims to investigate the significance of ANXA3 expression and the mechanism by which ANXA3 is involved in the epithelial–mensenchymal transition (EMT) of gastric cancer cells.ResultsOur results confirmed that ANXA3 was high expression at the mRNA and protein level in GC cancer tissues and the majority of GC cell lines. In clinicopathological analysis, we found that increased expression of ANXA3 in tumors was closely associated with a poor prognosis. Xogenous ANXA3 transduction promoted proliferation, clone formation, migration, and invasion. Small interfering RNA silencing of ANXA3 inhibited these processes. Silence of ANXA3 inhibited tumorigenicity in vivo. Additionally, ANXA3 expression is associated with the epithelial–mesenchymal transition.MethodsFirstly, we investigated the ANXA3 expression on mRNA and protein level with RT-PCR and Western blot. Secondly, 183 GC patients tissues were used the to evaluate the clinicopathological characteristics and prognosis through immunohistochemistry. Furthermore, The functions of ANXA3 were analyzed in the cell proliferation, Colony Formation, migration, invasion and apoptosis of GC cell lines.ConclusionsOur research suggests that ANXA3 plays important roles in gastric cancer carcinogenesis and metastasis, and provides a valuable prognostic marker and potential target for treatment of gastric cancer patients.

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Decreased annexin A3 expression correlates with tumor progression in papillary thyroid cancer

Abstract: Decreased expression of ANXA3 in papillary thyroid cancer supports the idea that ANXA3 may be an effective marker of microcarcinoma, and a negative predictor of papillary thyroid cancer progression.

Cited by 31 publications

References 24 publications

The MiR-495/Annexin A3/P53 Axis Inhibits the Invasion and EMT of Colorectal Cancer Cells

The MiR-495/Annexin A3/P53 Axis Inhibits the Invasion and EMT of Colorectal Cancer Cells

Protein expression of nucleophosmin, annexin A3 and nm23-H1 correlates with human nasopharyngeal carcinoma radioresistance in vivo

Overexpression of ANXA3 is an independent prognostic indicator in gastric cancer and its depletion suppresses cell proliferation and tumor growth

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