Up-regulated of Angiopoietin-Like Protein 4 Predicts Poor Prognosis in Cervical Cancer

Nie, Dan; Zheng, Qianwen; Liu, Ling; Mao, Xiguang; Li, Zhengyu

doi:10.7150/jca.29916

Cited by 21 publications

(21 citation statements)

References 30 publications

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“…Previous studies demonstrated that ANGPTL4 was associated with a variety types of cancers such as osteosarcoma, 16 gastric cancer, 17 renal cell carcinoma, 18 non-small cell lung cancer, 19 and cervical cancer, 20 and played pivotal roles in tumor growth, proliferation and metastasis. 21 ANGPTL4 was identified as a factor of lipid metabolism and angiogenesis which could be regulated by the nuclear hormone receptors PPARs, hypoxic conditions, fasting, and transforming growth factor β.…”

Section: Discussionmentioning

confidence: 99%

“…[26][27][28][29] More importantly, ANGPTL4 was suggested to be a novel diagnostic and prognostic biomarker for patients with renal cell carcinoma or cervical cancer. 20,30 However, no reports have investigated the role of ANGPTL4 in PTC. Therefore, this study further explores the possibility of ANGPTL4 as a potential molecular target for thyroid cancer treatment.…”

Section: Discussionmentioning

confidence: 99%

“…It is reported that ANGPTL4 promotes the migration and differentiation of endothelial cell, leading to the formation of new blood vessels. 14,15 The expression of ANGPTL4 was increased in several solid tumors such as osteosarcoma, 16 gastric cancer, 17 renal cell carcinoma, 18 non-small cell lung cancer, 19 cervical cancer 20 and so on compared with corresponding paracancerous tissues. ANGPTL4 was identified as pro-tumorigenic protein, including stimulating tumor cell growth and proliferation, promoting tumor metastasis.…”

Section: Introductionmentioning

confidence: 99%

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<p>ANGPTL4 Promotes the Proliferation of Papillary Thyroid Cancer via AKT Pathway</p>

Yang¹,

Wang²,

Sun³

et al. 2020

OTT

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Although papillary thyroid carcinoma (PTC) is associated with a generally favorable prognosis, about 15% of patients present recurrence and distant metastasis in the next decade leading to death. Angiopoietin-like 4 (ANGPTL4) is secreted to circulation and belongs to the angiopoietin-like proteins. The expression of ANGPTL4 was increased in several solid tumor tissues compared to corresponding paracancerous tissues. ANGPTL4 was identified as pro-tumorigenic protein, including stimulating tumor cell growth, promoting tumor metastasis. However, the clinical significance and biological function of ANGPTL4 in PTC is still unclear. Hence, the purpose of this study was to evaluate the role of ANGPTL4 in PTC, investigating the possibility of whether ANGPTL4 could become a novel target for PTC therapy. Methods: We investigated the expression level of ANGPTL4 and pAKT in PTC and paracancerous tissue by immunohistochemistry. We determined the effect of ANGPTL4 in PTC cell proliferation through cell counting kit-8 (CCK-8) and cell cycle by flow cytometry analysis. Furthermore, the correlation between ANGPTL4 expression levels and PTC cell proliferation from the TCGA data set was analyzed by GSEA. We explored the role of ANGPTL4 on the phosphorylation of AKT and proliferation in PTC cells via overexpression or knockdown assays and AKT inhibitor assay. Results: In the present study, we found that ANGPTL4 was highly expressed in both protein and mRNA level in PTC compared with adjacent noncancerous tissues or benign nodule. ANGPTL4 expression increased according to thyroid tumor progression. ANGPTL4 level was positively correlated with the size of PTC. ANGPTL4 increased cell proliferation and decreased cell cycle arrest of PTC. Knockdown of ANGPTL4 inhibited the phosphorylation of AKT. ANGPTL4 regulated PTC cell proliferation through AKT signaling pathway. Conclusion: Our findings suggested that ANGPTL4 was increased in PTC compared with adjacent noncancerous tissues, and ANGPTL4 increased cell proliferation and inhibited cell cycle arrest in PTC cells via promoting AKT phosphorylation. The study may provide fundamental information to suggest its suitability as a target for the treatment of PTC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

<p>ANGPTL4 Promotes the Proliferation of Papillary Thyroid Cancer via AKT Pathway</p>

Yang¹,

Wang²,

Sun³

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…Knockdown of ANGPTL4 reportedly suppresses adenylate energy charge elevation, thus delaying EMT [26]. Upregulation of ANGPTL4 is associated with a poor prognosis of cancers and promotes tumor cell proliferation and migration, including OS cells [27,28]. STC1, as well as STC2, was originally identified as a calcium/phosphate-regulating hormone.…”

Section: Discussionmentioning

confidence: 99%

LAIR-1 overexpression inhibits epithelial–mesenchymal transition in osteosarcoma via GLUT1-related energy metabolism

et al. 2020

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Background: Leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1) is a collagen receptor belonging to the immunoglobulin superfamily. Although previous studies have evaluated the biological role of LAIR in solid tumors, the precise mechanisms underlying the functions of LAIR-1 as a regulator of tumor biological functions remain unclear. Methods: LAIR-1 expression was evaluated by immunohistochemical analysis using an osteosarcoma (OS) tissue microarray. Wound healing and transwell migration assays were performed to evaluate tumor cell migration. Quantitative real-time polymerase chain reaction (qPCR) and western blotting were conducted to detect the expression of epithelial-mesenchymal transition (EMT)-related molecules. RNA-sequencing (RNA-seq) was conducted to evaluate the mRNA expression profiles after overexpressing LAIR-1 in OS cells. Glucose transporter (Glut)1 expression in OS cells was evaluated by western blotting. Results: LAIR-1 expression was significantly different between the T1 and T2 stages of OS tumors, and it inhibited OS cell migration. LAIR-1 expression was inversely correlated with the expression of Twist1, an EMT-associated transcription factor, via the Forkhead box O1 signal transduction pathway. Furthermore, RNA-seq and qPCR demonstrated that the expression of EMT energy metabolism-related molecules was significantly reduced after LAIR-1 overexpression. Conclusions: LAIR-1 overexpression decreased the expression of Glut1 and inhibited the expression of EMT-related molecules in OS cells. These findings provide new insights into the molecular mechanism underlying OS progression.

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“…Knockdown of ANGPTL4 reportedly suppresses adenylate energy charge elevation, thus delaying EMT [26]. Upregulation of ANGPTL4 is associated with a poor prognosis of cancers and promotes tumor cell proliferation and migration, including OS cells [27,28]. STC1, as well as STC2, was originally identi ed as a calcium/phosphate-regulating hormone.…”

Section: Discussionmentioning

confidence: 99%

LAIR-1 overexpression inhibits epithelial–mesenchymal transition in osteosarcoma via GLUT1-related energy metabolism

Zhang

Cheng

et al. 2020

Preprint

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Background: Leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1) is a collagen receptor belonging to the immunoglobulin superfamily. Although previous studies have evaluated the biological role of LAIR in solid tumors, the precise mechanisms underlying the functions of LAIR-1 as a regulator of tumor biological functions remain unclear.Methods: LAIR-1 expression was evaluated by immunohistochemical analysis using an osteosarcoma (OS) tissue microarray. Wound healing and transwell migration assays were performed to evaluate tumor cell migration. Quantitative real-time polymerase chain reaction (qPCR) and western blotting were conducted to detect the expression of epithelial–mesenchymal transition (EMT)-related molecules. RNA-sequencing (RNA-seq) was conducted to evaluate the mRNA expression profiles after overexpressing LAIR-1 in OS cells. Glucose transporter (Glut)1 expression in OS cells was evaluated by western blotting.Results: LAIR-1 expression was significantly different between the T1 and T2 stages of OS tumors, and it inhibited OS cell migration. LAIR-1 expression was inversely correlated with the expression of Twist1, an EMT-associated transcription factor, via the Forkhead box O1 signal transduction pathway. Furthermore, RNA-seq and qPCR demonstrated that the expression of EMT energy metabolism-related molecules was significantly reduced after LAIR-1 overexpression.Conclusions: LAIR-1 overexpression decreased the expression of Glut1 and inhibited the expression of EMT-related molecules in OS cells. These findings provide new insights into the molecular mechanism underlying OS progression.

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Up-regulated of Angiopoietin-Like Protein 4 Predicts Poor Prognosis in Cervical Cancer

Cited by 21 publications

References 30 publications

<p>ANGPTL4 Promotes the Proliferation of Papillary Thyroid Cancer via AKT Pathway</p>

<p>ANGPTL4 Promotes the Proliferation of Papillary Thyroid Cancer via AKT Pathway</p>

LAIR-1 overexpression inhibits epithelial–mesenchymal transition in osteosarcoma via GLUT1-related energy metabolism

LAIR-1 overexpression inhibits epithelial–mesenchymal transition in osteosarcoma via GLUT1-related energy metabolism

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