Angiopoietin-like 4 promotes osteosarcoma cell proliferation and migration and stimulates osteoclastogenesis

Zhang, T.; Kastrenopoulou, Afroditi; Larrouture, Quitterie C.; Athanasou, Nicholas A.; Knowles, Helen J.

doi:10.1186/s12885-018-4468-5

Cited by 33 publications

(45 citation statements)

References 64 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%

“…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: Introductionmentioning

confidence: 99%

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

Yang¹,

Wang²,

Sun³

et al. 2020

OTT

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“…HIF‐1α functions importantly in promoting tumor metastasis and proliferation . We investigated the function of HIF‐1α in circPIP5K1A/miR‐600‐mediated NSCLC cell proliferation and migration.…”

Section: Resultsmentioning

confidence: 99%

“…HIF-1α functions importantly in promoting tumor metastasis and proliferation. [22][23][24] We investigated the function of HIF-1α in circPIP5K1A/miR-600-mediated NSCLC cell proliferation and migration. Bifluorescein reporter detection showed that cotransfection of miR-600 mimics and reporter plasmids (including the HIF-1α 3′-UTR) decreased luciferase activity, whereas cotransfection with miR-600 mimics and mutated vectors verified that there was no obvious effect on luciferase activity.…”

Section: The Mir-600 Targets the Hif-1α Gene 3′-utrmentioning

confidence: 99%

Circular RNA circPIP5K1A promotes non‐small cell lung cancer proliferation and metastasis through miR‐600/HIF‐1α regulation

Chi

Luo

Song

et al. 2019

J of Cellular Biochemistry

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Circular RNAs (circRNAs) have an important function in human diseases, especially in cancer. circRNA hsa_circ_0014130 (circPIP5K1A), a particularly abundant circRNA, participates in the tumorigenesis of non‐small cell lung cancer (NSCLC), although the underlying regulatory mechanism remains unclear. Here, we investigated the circPIP5K1A role in NSCLC. Expression of circPIP5K1A in NSCLC cell lines was explored with quantitative real‐time PCR. The effect of circPIP5K1A on NSCLC was evaluated with circPIP5K1A silencing, miR‐600 mimic transfection, and hypoxia‐inducible factor (HIF)‐1α overexpression, followed by assessment of cell proliferation, metastasis, and tumorigenesis in nude mice. The subcellular localization of circPIP5K1A was evaluated via fluorescence in situ hybridization (FISH), and correlation between circPIP5K1A, miR‐600, and HIF‐1α was assessed by luciferase assay. The data demonstrated that circPIP5K1A expression was increased in NSCLC cells. FISH showed that circPIP5K1A localized to the cytoplasm. The circPIP5K1A knockdown suppressed NSCLC cell metastasis and proliferation by promoting expression of miR‐600. Overexpression of miR‐600 inhibited HIF‐1α‐mediated metastasis and proliferation of NSCLC cell by downregulating the endothelial mesenchymal transition‐related proteins, Snail and vimentin, and upregulating E‐cadherin. In vivo experiments illustrated that circPIP5K1A silence suppressed tumor growth and pulmonary metastasis. The circPIP5K1A may function as an miR‐600 sponge to facilitate NSCLC proliferation and metastasis by promoting HIF‐1α. A bifluorescein reporter experiment confirmed that miR‐600 was the circPIP5K1A target, and miR‐600 interacted with the 3′ untranslated region of HIF‐1α. These results show that circPIP5K1A acted as a tumor promoter through a novel circPIP5K1A/miR‐600/HIF‐1α axis, which provides candidate markers and therapeutic targets for NSCLC.

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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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Angiopoietin-like 4 promotes osteosarcoma cell proliferation and migration and stimulates osteoclastogenesis

Cited by 33 publications

References 64 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>

Circular RNA circPIP5K1A promotes non‐small cell lung cancer proliferation and metastasis through miR‐600/HIF‐1α regulation

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

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