Overexpression of AKIP1 promotes angiogenesis and lymphangiogenesis in human esophageal squamous cell carcinoma

Lin, Chuyong; Song, Libing; Liu, Aibin; Gong, Hui; Lin, Xi; Wu, Jueheng; Li, M; Li, J

doi:10.1038/onc.2013.559

Cited by 51 publications

(56 citation statements)

References 42 publications

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“…A‐kinase‐interacting protein 1, is a nuclear protein whose transcripts are differentially expressed in different cells and tissues, and it is initially found highly expressed in the cell lines of breast cancer and prostate cancer . Despite the biochemical or biological functions of AKIP1 is not well illuminated, the influence of AKIP1 on cancer cells have been illuminated by several studies . For example, a study reveals that AKIP1 transcriptionally upregulates vascular endothelial growth factor‐C (VEGF‐C) by cooperating with several transcriptional factors such as specificity protein 1 (Sp1), activator protein 2 (AP2), and NF‐kB, thereby enhances angiogenesis and lymphangiogenesis in human esophageal squamous cell carcinoma .…”

Section: Discussionmentioning

confidence: 99%

“…10,14,15 Despite the biochemical or biological functions of AKIP1 is not well illuminated, the influence of AKIP1 on cancer cells have been illuminated by several studies. 8,9,16 For example, a study reveals that AKIP1 transcriptionally upregulates vascular endothelial growth factor-C (VEGF-C) by cooperating with several transcriptional factors such as specificity protein 1 (Sp1), activator protein 2 (AP2), and NF-kB, thereby enhances angiogenesis and lymphangiogenesis in human esophageal squamous cell carcinoma. 9 Also, a study displays that AKIP1 upregulates the expression of chemokine (C-X-C motif) ligand 1 (CXCL1), CXCL2 and CXCL8 via activating IKKβ/NF-κB signaling pathway, and thus contributes to cell proliferation in cervical cancer cells, which further facilitates angiogenesis as well as enhances tumor growth in BALB/c nude mouse xenograft model.…”

Section: Discussionmentioning

confidence: 99%

“…9,16 For instance, a previous study displays that AKIP1 is overexpressed in clinical esophageal squamous cell carcinoma samples, and its expression is positively correlated with TNM stage in ESCC patients. 9 Another study discloses that AKIP1 is overexpressed in breast cancer tissues compared to normal breast tissues, and its high expression correlates with advanced tumor stage as well as lymph node metastasis in breast cancer patients. 16 These studies reveal that AKIP1 is upregulated in tumor tissues of several cancers, and its high expression is associated with increased disease progression in these cancer patients, whereas evidence about the correlation of AKIP1 expression with clinical characteristics in NSCLC patients is limited, only a study with small sample size displayed a positive correlation of AKIP1 expression with some tumor features, which needs to be further validated.…”

Section: Discussionmentioning

confidence: 99%

“…A‐kinase‐interacting protein 1 (AKIP1) is 23‐kDa protein that localizes in the cytoplasm, nucleus, and mitochondria, and it serves as an adaptor of intracellular structural protein . Limited studies have displayed that AKIP1 is upregulated in tumor cells or tumor tissues such as colorectal cancer, cervical cancer, and esophageal squamous cell carcinoma, and its overexpression associates with abnormal physiological and pathological changes in patients with these cancers, indicating that AKIP1 may behave as an oncogene in these cancers . Moreover, AKIP1 has been reported to act as a molecular determinant of protein kinase (PKA) in nuclear factor‐kB (NF‐κB) signaling, which is an inducible transcriptional factor for genes involved in inflammatory responses and cell proliferation in many diseases, particular in cancers .…”

Section: Introductionmentioning

confidence: 99%

“…[5][6][7] Limited studies have displayed that AKIP1 is upregulated in tumor cells or tumor tissues such as colorectal cancer, cervical cancer, and esophageal squamous cell carcinoma, and its overexpression associates with abnormal physiological and pathological changes in patients with these cancers, indicating that AKIP1 may behave as an oncogene in these cancers. 8,9 Moreover, AKIP1 has been reported to act as a molecular determinant of protein kinase (PKA) in nuclear factor-kB (NF-κB) signaling, which is an inducible transcriptional factor for genes involved in inflammatory responses and cell proliferation in many diseases, particular in cancers. 10,11 For NSCLC, Guo et al 12 reveal that overexpression of AKIP1 in NSLCC tissues was positively correlated with tumor features and AKIP promoted epithelial-mesenchymal transition (EMT) of NSCLC via transactivating zinc finger E-box binding homeobox 1 (ZEB1), while the sample size of 139 was relatively low, which might result in low statistical efficacy, and no further study was found to verify their results.…”

Section: Introductionmentioning

confidence: 99%

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A‐kinase‐interacting protein 1 overexpression correlates with deteriorative tumor features and worse survival profiles, and promotes cell proliferation but represses apoptosis in non‐small‐cell lung cancer

Chen

Yan

Liu

et al. 2019

Clinical Laboratory Analysis

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Background This study aimed to explore the correlation of A‐kinase‐interacting protein 1 (AKIP1) expression with clinical characteristics as well as survival profiles in non‐small‐cell lung cancer (NSCLC) patients, and further investigate its underlying effect on regulating NSCLC cell functions. Methods 319 NSCLC patients who underwent resection were consecutively reviewed, and AKIP1 expression (in 319 tumor tissues and 145 adjacent tissues) was determined by immunohistochemistry. Disease‐free survival (DFS) and overall survival (OS) were calculated. In vitro, control overexpression, AKIP1 overexpression, control shRNA and AKIP1 shRNA plasmids were transfected into A549 cells to evaluate the effect of AKIP1 on cell proliferation and apoptosis. Results A‐kinase‐interacting protein 1 expression was increased in tumor tissues compared to adjacent tissues, and it positively correlated with tumor size, lymph node metastasis and TNM stage in NSCLC patients. Kaplan‐Meier curves displayed that AKIP1 high expression correlated with worse DFS and OS, and multivariate Cox's regression revealed that it was an independent predictive factor for poor survival profiles. In vitro experiments displayed that AKIP1 expression was elevated in PC9 and A549 cells compared to normal lung epithelial cells; moreover, cell proliferation was increased by AKIP1 upregulation but reduced by AKIP1 downregulation, and cell apoptosis was decreased by AKIP1 upregulation but increased by AKIP downregulation in A549 cells. Interestingly, AKIP1 promoted fibronectin and zinc finger E‐box binding homeobox 1 expressions while reduced E‐cadherin expression in A549 cells. Conclusion A‐kinase‐interacting protein 1 overexpression correlates with deteriorative tumor features and worse survival profiles and promotes cell proliferation but represses apoptosis in NSCLC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

A‐kinase‐interacting protein 1 overexpression correlates with deteriorative tumor features and worse survival profiles, and promotes cell proliferation but represses apoptosis in non‐small‐cell lung cancer

Chen

Yan

Liu

et al. 2019

Clinical Laboratory Analysis

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ANP32E induces tumorigenesis of triple‐negative breast cancer cells by upregulating E2F1

Xiong

et al. 2018

Molecular Oncology

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Triple‐negative breast cancer (TNBC) lacks expression of estrogen receptor (ER), progesterone receptor, and the HER2 receptor; it is highly proliferative and becomes the deadliest forms of breast cancer. Effective prognostic methods and therapeutic targets for TNBC are required to improve patient outcomes. Here, we report that acidic nuclear phosphoprotein 32 family member E (ANP32E), which promotes cell proliferation in mammalian development, is highly expressed in TNBC cells compared to other types of breast cancer. High expression of ANP32E correlates significantly with worse overall survival (OS; P < 0.001) and higher risks of disease recurrence (P < 0.001) in patients with TNBC. Univariate and multivariate Cox‐regression models show that ANP32E is an independent prognostic factor in TNBC. Furthermore, we discovered that ANP32E promotes tumor proliferation in vitro by inducing G1/S transition, and ANP32E inhibition suppresses tumor formation in vivo. By examining the expression of E2F1, cyclin E1, and cyclin E2, we discovered that ANP32E promotes the G1/S transition by transcriptionally inducing E2F1. Taken together, our study shows that ANP32E is an efficient prognostic marker, and it promotes the G1/S transition and induces tumorigenesis of TNBC cells by transcriptionally inducing E2F1.

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Identification of A‐kinase interacting protein 1 as a potential biomarker for risk and prognosis of acute myeloid leukemia

Yan¹,

Li²,

Gao³

2020

Clinical Laboratory Analysis

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractBackground: This study aimed to investigate the correlation of A-kinase interacting protein 1 (AKIP1) expression with disease risk, clinical characteristics, and prognosis of acute myeloid leukemia (AML).Methods: 291 de novo AML patients and 97 controls were consecutively recruited, and bone marrow samples were collected to detect AKIP1 expression using quantitative polymerase chain reaction prior to initial treatment. Treatment response, eventfree survival (EFS), and overall survival (OS) in AML patients were evaluated. Results:A-kinase interacting protein 1 expression was higher in AML patients than that in controls; meanwhile, receiver operating characteristic curve displayed that AKIP1 was able to distinguish AML patients from controls (area under the curve:0.772, 95%CI: 0.720-0.823). Among AML patients, AKIP1 high expression was correlated with −7 or 7q−, monosomal karyotype, and worse risk stratification. Moreover, AKIP1 expression was negatively correlated with complete remission achievement, while no correlation of AKIP1 expression with hematopoietic stem cell transplantation achievement was observed. AKIP1 high expression was associated with shorter EFS and OS in total patients, and further subgroup analysis exhibited that AKIP1 high expression correlated with worse EFS and OS in intermediate-risk and poor-risk patients but not in better-risk patients. Besides, subsequent analysis revealed that AKIP1 high expression was an independent factor predicting unfavorable EFS and OS. Conclusion:A-kinase interacting protein 1 has the potential to be a novel marker for assisting AML management. K E Y W O R D S acute myeloid leukemia, A-kinase interacting protein 1, risk stratification, survival 1 | INTRODUC TI ON Acute myeloid leukemia (AML), an aggressive hematological malignancy, is characterized by abnormal cell proliferation and differentiation of the immature myeloid cells. 1,2 It accounts for 20% of all hematological malignancy related deaths, with a 5-year survival rate of 40% for younger patients (18-60 years) and 5-year survival rate of 10% for the elder patients (age above 60 years). 3-5 Despite there are potentially curative treatments for AML patients, including intensive chemotherapy and allogeneic stem cell transplantation, How to cite this article: Yan Y, Li X, Gao J. Identification of A-kinase-interacting protein 1 as a potential biomarker for risk and prognosis of acute myeloid leukemia. J Clin Lab Anal.

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Overexpression of AKIP1 promotes angiogenesis and lymphangiogenesis in human esophageal squamous cell carcinoma

Cited by 51 publications

References 42 publications

A‐kinase‐interacting protein 1 overexpression correlates with deteriorative tumor features and worse survival profiles, and promotes cell proliferation but represses apoptosis in non‐small‐cell lung cancer

A‐kinase‐interacting protein 1 overexpression correlates with deteriorative tumor features and worse survival profiles, and promotes cell proliferation but represses apoptosis in non‐small‐cell lung cancer

ANP32E induces tumorigenesis of triple‐negative breast cancer cells by upregulating E2F1

Identification of A‐kinase interacting protein 1 as a potential biomarker for risk and prognosis of acute myeloid leukemia

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