Collagen triple helix repeat containing 1 (Cthrc1) is an independently prognostic biomarker of non-small cell lung cancers with cigarette smoke

Liu, Xiaojun; Liu, Beiyan; Cui, Ying; Wang, Fengping; Sun, Hui; Lv, Fuzhen

doi:10.1007/s13277-014-2449-0

Cited by 10 publications

(8 citation statements)

References 24 publications

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“…Naturally, many other genes as MMP family [ 40 ] and Cthrc1 [ 24 ] have been demonstrated to associate with NSCLC invasion and metastasis during the ongoing researches of NSCLC. Based on bioinformatics analysis, we detected the Cthrc1 mRNA expression and found elevated expression of Cthrc1 was also associated with the occurrence of the differentiation status, TNM stage and lymph node metastases in NSCLC patients, and Pearson correlation analysis indicated that the expression of miR-30b and Cthrc1 mRNA were inversely correlated.…”

Section: Discussionmentioning

confidence: 99%

“…MiR-30b is a member of the miR-30 family, which plays an important regulatory role in the development of several cancers including breast cancer [ 16 ], malignant peripheral nerve sheath tumors [ 17 ], glioma [ 18 ] and lung cancer [ 19 ]. Collagen triple helix repeat containing 1 (Cthrc1) has also been associated with the development of certain cancers, including lung cancer [ 20 – 24 ], therefore we decided to explore a possible interaction between miR-30b and Cthrc1 and the potential significance in the invasion and metastasis of NSCLC.…”

Section: Introductionmentioning

confidence: 99%

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microRNA-30b inhibits cell invasion and migration through targeting collagen triple helix repeat containing 1 in non-small cell lung cancer

Chen

Yang

et al. 2015

Cancer Cell Int

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BackgroundNon-small cell lung cancer (NSCLC) is the largest histological subgroup of lung cancer and has increased in prevalence in China over the past 5 years. The 5-year survival rate has remained at 15–20 %, with a median survival of 8–12 months. The tumorigenesis and progression of NSCLC is orchestrated by numerous oncogene and anti-oncogene mutations and insights into microRNA function have increased our understanding of the process. Here, we investigated the effects of miR-30b on NSCLC cell invasion and migration and explored the underlying molecular mechanisms involved.MethodsQuantitative reverse transcription PCR, wound healing assay, trans-well assays, western blotting and dual luciferase assays were performed to investigate the molecular mechanisms of miR-30b in NSCLC cells.ResultsMiR-30b was down-regulated and Cthrc1 up-regulated in NSCLC tissues. Both were associated with tumor differentiation, TNM stage and lymph node metastases. Up-regulation of miR-30b restricted A549 and Calu-3 cell invasion and migration. Additionally, the expression of Cthrc1, matrix metalloproteinase-9 and matrix metalloproteinase-2 was reduced, while metallopeptidase inhibitor-1 expression increased. Bioinformatics analysis identified Cthrc1 as a target of miR-30b and western blotting and luciferase reporter assays confirmed that miR-30b regulates Cthrc1 by directly binding to its 3′UTR. Transfection of Cthrc1 without the 3′UTR restored the miR-30b inhibiting cell invasion. Up-regulation of miR-30b or down-regulation of Cthrc1 had potential significance in the invasion and metastasis of NSCLC.ConclusionsMiR-30b was down-regulated and Cthrc1 up-regulated in NSCLC tissues. Both of them were related to tumor differentiation, TNM stage and lymph node metastases. MiR-30b affected NSCLC cells invasion and migration by regulating Cthrc1.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

microRNA-30b inhibits cell invasion and migration through targeting collagen triple helix repeat containing 1 in non-small cell lung cancer

Chen

Yang

et al. 2015

Cancer Cell Int

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“…Likewise, western blot, RT-PCR and immunofluorescence analyses results indicated that the expression of CTHRC1 in five NSCLC cell lines (NCI-H226, NCl-H23, NCl-H820, NCl-H446 and A549) was markedly stronger than that of normal human lung epithelial cells (Beas-2Bs) 11. Two independent analyses using lung cancer specimens revealed that overexpression of CTHRC1 strikingly associated with differentiation degree, clinical stage, T classification, lymph node metastasis, distant metastasis and cigarette smoke as well as with poor clinical survival time of the patients compared with patient with low CTHRC1 expression 11, 21. Furthermore, the observed results displayed that there were no significant differences between CTHRC1 and mRNA levels with different genders, ages or pathological types 22.…”

Section: Expression Profile In Several Representative Malignant Tumentioning

confidence: 97%

“…Recent research has explored the aberrant up-regulation of CTHRC1 in NSCLC 11, 21, 22, Ke al el showed that overexpression of CTHRC1 increased NSCLC proliferation, invasion and metastasis in vitro via the Wnt/β-catenin signaling pathway 11. Based on this observation, paraffin-embedded immunohistochemical analysis of CTHRC1 in NSCLC patient tissues (212/292, 72.60%) illustrated that the up-regulated levels of both mRNA and protein were evidently higher than those in the paired adjacent non-cancerous tissues (6/66, 9.09%) (p<0.001).…”

Section: Expression Profile In Several Representative Malignant Tumentioning

confidence: 99%

Multidimensional Roles of Collagen Triple Helix Repeat Containing 1 (CTHRC1) in Malignant Cancers

et al. 2016

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Tumor is one of the principal diseases that seriously threaten human health. Insight into sensitive cancer markers may open a new avenue for the early diagnosis and treatment of this disease. CTHRC1 has been identified as a cancer-related gene. It is a secretory glycoprotein that possesses multidimensional roles associated with wound repair, bone remodeling, hepatocytes fibrosis, adipose tissue formation, and so on. Our previous studies and numerous reports from other researchers have revealed that the ascended expression of CTHRC1 tends to go hand in hand with tumorigenesis, proliferation, invasion and metastasis in various human malignancies through a series of molecular mechanisms and signaling pathways. However, the detailed pathogenic mechanisms of CTHRC1 overexpression in human malignant cancers are not yet clear. Here, we shall focus our description on the functions, expression profile in several representative malignant tumors and a number of molecular mechanisms and signaling pathways involved with CTHRC1. This introductory discussion of CTHRC1 will serve as a reference for further research in understanding this intriguing cancer-related protein.

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“…It was demonstrated that Cthrc1 is related to vascular remodeling by inhibiting collagen production and fibrogenesis, and by promoting cell migration (8). The majority of Cthrc1 studies have focused on its effects and underlying molecular mechanism, in promoting tumor cell invasion and metastasis (9)(10)(11)(12)(13)(14). In the present study, it was demonstrated that increased expression of Cthrc1 protein in gastrointestinal stromal tumor (GIST) is associated with increased microvascular density (MVD) in a tissue microarray; however, to the best of our knowledge, no previous study has demonstrated the effect of Cthrc1 in endothelial angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

Collagen triple helix repeat containing 1 promotes tumor angiogenesis in gastrointestinal stromal tumors

Chen

Lin

et al. 2017

Oncol Lett

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Abstract. Collagen triple helix repeat containing 1 (Cthrc1) is a secreted protein that has been observed to lead to poorer prognosis by inducing the invasion and metastasis in different tumors; however, it has not been demonstrated that Cthrc1 is involved in tumor angiogenesis. Immunohistochemical staining of Cthrc1 and CD31 in gastrointestinal stromal tumor tissue demonstrated that Cthrc1 is associated with microvascular density. Overexpression of Cthrc1 protein may alter the properties of human umbilical vein endothelial cells (HUVECs), including migration, invasion, tubule formation and aortic ring sprouting. Small interfering RNA-mediated knockdown of Cthrc1 was performed to verify the opposite effects. Migration and tubule formation induced by Cthrc1 overexpression in HUVECs was attenuated by inhibition of phosphorylation in extracellular-signal-regulated protein kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways. The pro-angiogenic effect of Cthcr1 is associated with increased phosphorylation of ERK and JNK in HUVECs. Silencing the expression of Cthrc1 protein may be a promising strategy to inhibit tumor angiogenesis.

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Collagen triple helix repeat containing 1 (Cthrc1) is an independently prognostic biomarker of non-small cell lung cancers with cigarette smoke

Cited by 10 publications

References 24 publications

microRNA-30b inhibits cell invasion and migration through targeting collagen triple helix repeat containing 1 in non-small cell lung cancer

microRNA-30b inhibits cell invasion and migration through targeting collagen triple helix repeat containing 1 in non-small cell lung cancer

Multidimensional Roles of Collagen Triple Helix Repeat Containing 1 (CTHRC1) in Malignant Cancers

Collagen triple helix repeat containing 1 promotes tumor angiogenesis in gastrointestinal stromal tumors

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