Tumor-Suppressing Effect of Silencing of Annexin A3 Expression in Breast Cancer

Kim, Ju‐Yeon; Jung, Eun Jung; Park, Hyojin; Lee, Jeong-Hee; Song, Eun Jin; Kwag, Seung-Jin; Park, Ji-Ho; Park, Taejin; Jeong, Sang‐Ho; Jeong, Chi‐Young; Ju, Young‐Tae; Lee, Young-Joon; Hong, Soon Chan

doi:10.1016/j.clbc.2017.11.009

Cited by 15 publications

(18 citation statements)

References 21 publications

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“…Annexin A3 (ANXA3) belongs to the Annexin family, which are a well-known multigene family of membrane-binding proteins and Ca 2+ -regulated phospholipid proteins 7 . ANXA3 has been found to be correlated with cancer proliferation, colony-forming ability, invasion, and migration 8, 9. In this study, microarray-based gene expression analysis implied that ANXA3 was closely correlated with IA.…”

Section: Introductionmentioning

confidence: 87%

RETRACTED: ANXA3 Silencing Ameliorates Intracranial Aneurysm via Inhibition of the JNK Signaling Pathway

Wang

Yang

et al. 2019

Molecular Therapy - Nucleic Acids

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Intracranial aneurysm (IA) rupture is a major cause of stroke death. Alteration of vascular smooth muscle cell (VSMC) function and phenotypic modulation plays a role in aneurysm progression. In the present study, we investigated the role of Annexin A3 (ANXA3) silencing in IA with the interaction of the c-Jun N-terminal kinase (JNK) signaling pathway. In IA and VSMCs of IA, the relationship between ANXA3 and the JNK signaling pathway was verified. To investigate the specific mechanism of ANXA3 silencing in IA, we transfected VSMCs with the overexpressed or small interfering RNA (siRNA) of ANXA3, or treated them with an inhibitor of the JNK signaling (SP600125). Cell counting kit-8 (CCK-8) assay was conducted to detect cell viability, and flow cytometry was conducted to assess cell cycle and apoptosis so as to evaluate the gain- and loss-of-function of ANXA3 and investigate the involvement of the JNK signaling pathway. The aneurysm wall of IA cells demonstrated an elevated level of ANXA3 expression and an activated JNK signaling pathway. VSMCs treated with siRNA-ANXA3 or SP600125 showed decreased expression of JNK, caspase-3, osteopontin (OPN), Bax, and matrix metalloproteinase-9 (MMP-9), as well as phosphate (p)-JNK, but increased the expression of α smooth muscle actin (α-SMA), β-tubulin, and Bcl-2. ANXA3 silencing or inactivation of the JNK signaling pathway also enhanced proliferation and repressed apoptosis of VSMCs. Collectively, this study shows that the silencing of ANXA3 can rescue VSMC function in IAs by inhibiting the phosphorylation and activation of the JNK signaling pathway. These findings may provide a potential therapy for the molecular treatment of IAs.

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Section: Introductionmentioning

confidence: 87%

RETRACTED: ANXA3 Silencing Ameliorates Intracranial Aneurysm via Inhibition of the JNK Signaling Pathway

Wang

Yang

et al. 2019

Molecular Therapy - Nucleic Acids

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“…Aside from promoting the pro-proliferative pathways, aberrant expression of ANXA3 has also been shown to downregulate multiple pro-apoptotic proteins and cyclin-dependent kinases (CDKs), which facilitates the evasion of apoptosis and cell cycle arrest. For example, in vitro investigations on breast cancer cell lines HCC-1954 and MDA-MB-231 demonstrated that ANXA3 silencing using siRNA significantly reduced the expression of CDK4 and enhanced the expression of E2F1 and p27 Kip1 ( Kim et al, 2018 ). Furthermore, high levels of ANXA3 in hepatocellular carcinoma has been demonstrated to attenuate the PKCδ/p38 associated apoptosis ( Tong et al, 2018 ).…”

Section: The Role Of Anxa3 In Tumorigenesismentioning

confidence: 99%

“…Invasion and metastasis are the major cause of poor clinical outcomes of malignant diseases. In vitro investigations have revealed that ANXA3 overexpression significantly stimulated the invasion and migration of breast cancer cells ( Ibrahim et al, 2012 ; Guo et al, 2017 ; Kim et al, 2018 ). Clinically, ANXA3 overexpression has been demonstrated to be correlated with the occurrence of lymph node metastasis and the clinicopathological stages of breast cancer ( Zhou et al, 2017b ) and lung adenocarcinoma ( Liu et al, 2009 ).…”

Section: The Role Of Anxa3 In Tumorigenesismentioning

confidence: 99%

“…However, data published so far about its expression in different malignancies are inconsistent. To the best of our knowledge, ANXA3 has been reported to be overexpressed in a majority cancer types including breast ( Pendharkar et al, 2016 ; Zhou et al, 2017a ; Zhou et al, 2017b ; Guo et al, 2017 ; Aravind Kumar et al, 2018 ; Du et al, 2018 ; Kim et al, 2018 ; Li et al, 2018 ; Zhou et al, 2018 ), colorectal ( Madoz-Gurpide et al, 2006 ; Marshall et al, 2010 ; Yip et al, 2010 ; Yang L. et al, 2018 ; Yang Q. et al, 2018 ; Xu et al, 2019 ), bladder ( Tsai et al, 2018 ), ovarian ( Jiang et al, 2019 ), gastric ( Takahashi et al, 2015 ; Wang and Li, 2016 ) and pancreatic cancer ( Baine et al, 2011a ; Baine et al, 2011b ; Wan et al, 2020 ) as well as hepatocellular ( Pan et al, 2015a ; Pan et al, 2015b ; Tong et al, 2018 ) and nasopharyngeal carcinoma ( Ruan et al, 2010 ), while downregulated in renal ( Bianchi et al, 2010 ), prostate ( Wozny et al, 2007 ; Köllermann et al, 2008 ; Peraldo-Neia et al, 2011 ) and papillary thyroid cancer ( Jung et al, 2010 ). Furthermore, the expression of ANXA3 in lung cancer remains controversial, with the evidence of both upregulated ( Liu et al, 2009 ; Győrffy et al, 2013 ; Wang et al, 2019 ; Jin et al, 2020 ; Liu et al, 2021 ) and downregulated ( Rho et al, 2009 ; Wu et al, 2018 ; Lohinai et al, 2019 ) expression patterns documented in the literature.…”

Section: Introductionmentioning

confidence: 97%

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Annexin A3, a Calcium-Dependent Phospholipid-Binding Protein: Implication in Cancer

Liu

Yang

et al. 2021

Front. Mol. Biosci.

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Annexin A3 (ANXA3), also known as lipocortin III and placental anticoagulant protein III, has been reported to be dysregulated in tumor tissues and cancer cell lines, and harbors pronounced diagnostic and prognostic value for certain malignancies, such as breast, prostate, colorectal, lung and liver cancer. Aberrant expression of ANXA3 promotes tumor cell proliferation, invasion, metastasis, angiogenesis, and therapy resistance to multiple chemotherapeutic drugs including platinum-based agents, fluoropyrimidines, cyclophosphamide, doxorubicin, and docetaxel. Genetic alterations on the ANXA3 gene have also been reported to be associated with the propensity to form certain inherited, familial tumors. These diverse functions of ANXA3 in tumors collectively indicate that ANXA3 may serve as an attractive target for novel anticancer therapies and a powerful diagnostic and prognostic biomarker for early tumor detection and population risk screening. In this review, we dissect the role of ANXA3 in cancer in detail.

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“…Next, 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) was added to each well at a final concentration of 0.5 mg/mL for 4 h. The supernatants were transferred, dimethyl sulfoxide (DMSO) was added and the absorbance of each well was measured at 490 nm using an ELISA microplate reader (Bio-Rad, Hercules, CA, USA) (33).…”

Section: Cell Proliferation Assaysmentioning

confidence: 99%

Downregulation of NCL attenuates tumor formation and growth in cervical cancer by targeting the PI3K/AKT pathway

Ying

R²,

Tang

et al. 2021

Preprint

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Nucleolin (NCL, C23) is a multifunctional phosphoprotein that plays a vital role in modulating the survival, proliferation and apoptosis of cancer cells. However, the effects of NCL on cervical cancer and the underlying mechanisms behind this are poorly understood. In the study presented here, Hela cells were transfected with shRNAs targeting the endogenous NCL gene (sh-NCL-Hela). NCL knockdown inhibited cell proliferation and promoted apoptosis both in vivo and in vitro. Mechanistic studies revealed that NCL knockdown inhibited the PI3K/AKT pathway by upregulating FGF, ITGA, TNXB, VEGF, Caspase 3, and Bax, as well as by downregulating AKT, GNB4, CDK6, IL6R, LAMA, PDGFD, PPP2RSA and BCL-2. In addition, the expression levels of apoptosis-related genes after using a PI3K inhibitor LY294002 were consistent with shRNA studies, while treatment with a 740Y-P agonist showed the opposite effect. Altogether, this study uncovered that downregulation of NCL may be a novel treatment strategy for cervical cancer.

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Tumor-Suppressing Effect of Silencing of Annexin A3 Expression in Breast Cancer

Cited by 15 publications

References 21 publications

RETRACTED: ANXA3 Silencing Ameliorates Intracranial Aneurysm via Inhibition of the JNK Signaling Pathway

RETRACTED: ANXA3 Silencing Ameliorates Intracranial Aneurysm via Inhibition of the JNK Signaling Pathway

Annexin A3, a Calcium-Dependent Phospholipid-Binding Protein: Implication in Cancer

Downregulation of NCL attenuates tumor formation and growth in cervical cancer by targeting the PI3K/AKT pathway

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