Impact of Annexin A3 expression in gastric cancer cells

Yu, Shan; Y, Li; Fan, Ling; Zhao, Qun; Bb, Tan; Y, Liu

doi:10.4149/neo_2014_033

Cited by 16 publications

(6 citation statements)

References 31 publications

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“…Numerous studies have reported that knockdown of ANXA3 reduces growth of lung adenocarcinoma, breast, and gastric cancer cells. [23][24][25] ANXA3 is inversely related to prognoses of patients with gastric cancer, and it positively regulates the expression of Bcl-2. 26 ANXA3 knockdown inhibits cell proliferation and facilitates apoptosis in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Annexin A3 depletion overcomes resistance to oxaliplatin in colorectal cancer via the MAPK signaling pathway

Yin

Zhang

et al. 2019

J of Cellular Biochemistry

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Colorectal cancer (CRC) is a common disease with high mortality and morbidity. Annexin A3 (ANXA3) belongs to the structurally homologous family of Ca2+ and phospholipid‐binding proteins. This study aimed to investigate the effects and potential mechanisms of ANXA3 on oxaliplatin (Ox) resistance in CRC. We generated two human CRC cell lines (HCT116/Ox and SW480/Ox) with acquired Ox resistance and determined their resistance properties. ANXA3 expression and cell apoptosis, migration and invasion also were evaluated. We found that cell viability of HCT116/Ox and SW480/Ox was higher than that in parental cells in the presence of Ox. ANXA3 was highly expressed in HCT116/Ox and SW480/Ox cells. ANXA3 downregulation diminished cell survival, migration and invasion, while increased the apoptosis of HCT116 and SW480 with or without Ox. Moreover, depletion of ANXA3 reduced cell viability and BrdU incorporation, increased cell apoptosis and c‐caspase 3 expression in HCT116/Ox with or without Ox. A transwell assay determined that knockdown of ANXA3 impeded the migration and invasion of HCT116/Ox and SW480/Ox cells. Additionally, phosphorylation of extracellular signal–regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) decreased upon ANXA3 depletion in HCT116/Ox cells, and ANXA3 silencing suppressed Ox‐induced activation of ERK and JNK signaling pathway. ANXA3 downregulation reduced Ox resistance in CRC, and treatment with the ERK inhibitor PD098059 or JNK inhibitor SP600125 contributed to this process. These results indicate that silencing ANXA3 could overcome Ox resistance in CRC via the mitogen‐activated protein kinase signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Annexin A3 depletion overcomes resistance to oxaliplatin in colorectal cancer via the MAPK signaling pathway

Yin

Zhang

et al. 2019

J of Cellular Biochemistry

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“…Studies have demonstrated that ANXA3 is a potential biomarker for carcinogenesis, metastasis and resistance to chemotherapy in many cancers such as ovarian cancer [11], gastric cancer [12], breast cancer [13, 14] and liver carcinoma [15, 16]. But there is hardly any investigation of its role in CRC.…”

Section: Discussionmentioning

confidence: 99%

High-throughput proteomics integrated with gene microarray for discovery of colorectal cancer potential biomarkers

Zhong

et al. 2016

Oncotarget

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Proteins, as executives of genes' instructions, are responsible for cellular phenotypes. Integrating proteomics with gene microarray, we conducted this study to identify potential protein biomarkers of colorectal cancer (CRC). Isobaric tags with related and absolute quantitation (iTRAQ) labeling mass spectrometry (MS) was applied to screen and identify differentially expressed proteins between paired CRC and adjacent normal mucosa. Meanwhile, Affymetrix U133plus2.0 microarrays were used to perform gene microarray analysis. Verification experiments included immunohistochemistry (IHC), western blot and enzyme-linked immunosorbent assay (ELISA) of selected proteins. Overall, 5469 differentially expressed proteins were detected with iTRAQ-MS from 24 matched CRC and adjacent normal tissues. And gene microarray identified 39859 differential genes from 52 patients. Of these, 3083 differential proteins had corresponding differentially expressed genes, with 245 proteins and their genes showed >1.5-fold change in expression level. Gene ontology enrichment analysis revealed that up-regulated proteins were more involved in cell adhesion and motion than down-regulated proteins. In addition, up-regulated proteins were more likely to be located in nucleus and vesicles. Further verification experiments with IHC confirmed differential expression levels of 5 proteins (S100 calcium-binding protein A9, annexin A3, nicotinamide phosphoribosyltransferase, carboxylesterase 2 and calcium activated chloride channel A1) between CRC and normal tissues. Besides, western blot showed a stepwise increase of annexin A3 abundance in normal colorectal mucosa, adenoma and CRC tissues. ELISA results revealed significantly higher serum levels of S100 calcium-binding protein A9 and annexin A3 in CRC patients than healthy controls, validating diagnostic value of these proteins. Cell experiments showed that inhibition of annexin A3 could suppress CRC cell proliferation and aggressiveness. S100 calcium-binding protein A9, annexin A3, nicotinamide phosphoribosyltransferase, carboxylesterase 2 and calcium activated chloride channel A1 were probably potential biomarkers of colorectal cancer. Annexin A3 was a potentially valuable therapeutic target of CRC.

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“…The above results indicated that Anxa3 downregulation could suppress the migration, invasion, and metastasis of LADC cells. Similarly, Yu et al reported that silencing endogenous Anxa3 suppressed the proliferation, migration, and invasion of gastric cancer cells [17]. As we know, MMP-2, E-cadherin, and N-cadherin are effector molecules with key roles in the migration and invasion of tumors [18–20].…”

Section: Discussionmentioning

confidence: 99%

Annexin A3 Knockdown Suppresses Lung Adenocarcinoma

Liu

Zhang

et al. 2016

Analytical Cellular Pathology

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Our previous study identified an elevated abundance of annexin A3 (Anxa3) as a novel prognostic biomarker of lung adenocarcinoma (LADC) through quantitative proteomics analysis. However, the biological functions of Anxa3 in LADC are not fully clear. In this study, in vitro and in vivo assays were performed to investigate the effects of Anxa3 downregulation on the growth, migration, invasion, metastasis, and signaling pathway activation of LADC cells. After Anxa3 downregulation, the growth of A549 and LTEP-a2 LADC cells was slowed and they showed decreased migration and invasion in vitro. Anxa3 knockdown significantly inhibited tumor formation by A549 cells in vivo; while many metastases were formed by control A549 cells, there were obvious reductions in the numbers of lung, liver, and brain metastases formed by Anxa3 knockdown in A549 cells. Furthermore, Anxa3 knockdown significantly decreased MMP-2 and N-cadherin expression and increased E-cadherin expression both in cell lines in vitro and in tumor nodules examined during in vivo tumorigenesis assays. Interestingly, Anxa3 downregulation reduced the phosphorylated levels of MEK and ERK. In summary, Anxa3 knockdown inhibited the growth, migration, invasion, and metastasis of LADC, decreased the activation of the MEK/ERK signaling pathway, and modulated the expression of MMP-2, E-cadherin, and N-cadherin.

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Impact of Annexin A3 expression in gastric cancer cells

Cited by 16 publications

References 31 publications

Annexin A3 depletion overcomes resistance to oxaliplatin in colorectal cancer via the MAPK signaling pathway

Annexin A3 depletion overcomes resistance to oxaliplatin in colorectal cancer via the MAPK signaling pathway

High-throughput proteomics integrated with gene microarray for discovery of colorectal cancer potential biomarkers

Annexin A3 Knockdown Suppresses Lung Adenocarcinoma

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