Collagen type XI α1 facilitates head and neck squamous cell cancer growth and invasion

Sok, John C.; Lee, J A; Dasari, Sumana; Joyce, Sonali; Contrucci, Sarah; Egloff, Ann Marie; Trevelline, Brian K.; Joshi, Radhika; Kumari, Niraj; Grandis, Jennifer R.; Thomas, Sufi M.

doi:10.1038/bjc.2013.624

Cited by 51 publications

(42 citation statements)

References 31 publications

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“…This finding was confirmed by another study in which colXIα1 was upregulated by an average of 6.63 fold in HNSCC tumors versus normal adjacent tissue 40 . An additional study demonstrated a 7.5-fold increase in colXI α1 mRNA levels in metastatic HNSCC tumors compared to non-metastatic tumors 41 .…”

Section: Dysregulation Of Collagen Xiα1 In Cancersupporting

confidence: 67%

“…ColXIα1 siRNA-mediated knockdown in both ovarian cancer cell lines and HNSCC cell lines significantly suppressed invasion and slowed proliferation. This effect was not observed when normal, non-cancerous cells were transfected with colXIα1 siRNA, further confirming its potential as a therapeutic target 28,40 . In the ovarian cancer cell lines, colXIα1 knockdown was associated with decreased matrix metalloproteinase (MMP) 3 mRNA expression and activity.…”

Section: Colxiα1 As a Therapeutic Targetmentioning

confidence: 74%

“…ColXIα1 was found to be more highly expressed by TAFs isolated from HNSCC explants than in normal fibroblasts derived from cancer-free patients 40 . Immunohistochemical studies in pancreatic cancer have also suggested that colXIα1 may be a marker capable of differentiating TAFs from normal activated fibroblasts, a distinction which has been elusive so far 47 .…”

Section: Colxiα1 and Tumor-associated Stromamentioning

confidence: 90%

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Tumor matrix protein collagen XIα1 in cancer

Raglow

Thomas

2015

Cancer Letters

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The extracellular matrix is increasingly recognized as an essential player in cancer development and progression. Collagens are one of the most important components of the extracellular matrix, and have themselves been implicated in many aspects of neoplastic transformation. Collagen XI is a minor collagen whose main physiologic function is to regulate the diameter of major collagen fibrils. The α1 chain of collagen XI (colXIα1), has known pathogenic roles in several musculoskeletal disorders. Recent research has highlighted the importance of colXIα1 in many types of cancer, including its roles in metastasis, angiogenesis, and drug resistance, as well as its potential utility in screening tests and as a therapeutic target. High levels of colXIα1 overexpression have been reported in multiple expression profile studies examining differences between cancerous and normal tissue, and between beginning and advanced stage cancer. Its expression has been linked to poor progression-free and overall survival. The consistency of this data across cancer types is particularly striking, including colorectal, ovarian, breast, head and neck, lung, and brain cancers. This review discusses the role of collagen XIα1 in cancer and its potential as a target for cancer therapy.

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Section: Dysregulation Of Collagen Xiα1 In Cancersupporting

confidence: 67%

Section: Colxiα1 As a Therapeutic Targetmentioning

confidence: 74%

Section: Colxiα1 and Tumor-associated Stromamentioning

confidence: 90%

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Tumor matrix protein collagen XIα1 in cancer

Raglow

Thomas

2015

Cancer Letters

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“…[18][19][20] For instance, in human acute lymphocytic leukemia, the expression levels of miR-15a and miR-16-1 are decreased; 21,22 in lung cancer, let-7 is downregulated, whereas miR-17-92 is upregulated; 23 in Burkitt's lymphoma, expression level of miR-155 is increased; 24 in esophageal cancer, miR-103 and miR-107 expression levels are increased; 25 in liver cancer, miR-21 expression level is increased. 26 The important roles of those miRs with altered expression have further been revealed, which forms the basis of their applications in clinical tumor treatments. 24,27 MiR played its role on the target gene through two ways, one was completely complementary pairing with the target gene that might lead to the degradation of the mRNA of the target gene and the other was incompletely complementary pairing with the target gene that might lead to translation inhibition of the target gene.…”

Section: Discussionmentioning

confidence: 99%

miR-15b regulates cisplatin resistance and metastasis by targeting PEBP4 in human lung adenocarcinoma cells

et al. 2015

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MicroRNAs (miRNAs) have been identified as important posttranscriptional regulators involved in various biological and pathological processes of cells, but their association with tumor chemoresistance has not been fully understood. We detected miR-15b expression in two lung adenocarcinoma cell lines, A549 and A549/CDDP, and then investigated the effects of miR-15b on the metastasis and the chemosensitivity of cancer cells, using both gain- and loss-of-function studies. The correlation between miR-15b level and chemoresistance was further investigated in clinical lung adenocarcinoma specimens. miR-15b was significantly upregulated in cisplatin-resistant lung adenocarcinoma A549/CDDP cells compared with parental A549 cells. miR-15b regulates epithelial-mesenchymal transition (EMT) and cisplatin resistance in vitro and modulates response of lung adenocarcinoma cells to cisplatin in vivo. Further studies identified phosphatidylethanolamine-binding protein 4 (PEBP4) as a direct and functional target of miR-15b. Small-interfering RNA-mediated PEBP4 knockdown revealed similar effects as that of ectopic miR-15b expression, whereas overexpression of PEBP4 attenuated the function of miR-15b in lung adenocarcinoma cells. Increased miR-15b expression was also detected in tumor tissues sampled from lung adenocarcinoma patients treated with cisplatin-based chemotherapy and was proved to be correlated with low expression of PEBP4, decreased sensitivity to cisplatin and poor prognosis. Our results suggest that upregulation of miR-15b could suppress PEBP4 expression and in turn contribute to chemoresistance of lung adenocarcinoma cells to cisplatin.

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“…Mutations of COL11A1 are also associated with type II Stickler syndrome and Marshall syndrome (17,18). In regard to tumor formation and development, COL11A1 was reported to promote tumor progression in ovarian cancer, and head and neck squamous cell cancer (HNSCC) (19)(20)(21) (22,23). However, the role of COL11A1 in NSCLC progression and relapse remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

COL11A1 is overexpressed in recurrent non-small cell lung cancer and promotes cell proliferation, migration, invasion and drug resistance

et al. 2016

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Abstract. Collagen type XI α1 (COL11A1), a minor fibrillar collagen, has been demonstrated to be involved in cell proliferation, migration and the tumorigenesis of many human malignancies. Previous studies have shown that COL11A1 may be a valuable diagnostic marker for non-small cell lung carcinoma (NSCLC). However, its biological function in NSCLC progression remains largely unclear. In the present study, we investigated the expression levels of COL11A1 in different human NSCLC samples, and found that COL11A1 was overexpressed in NSCLC with lymph node metastasis and in recurrent NSCLC tissues. We also revealed that COL11A1 promoted the cell proliferation, migration and invasion of NSCLC cell lines in vitro. Furthermore, our results highlighted the importance of COL11A1 in chemoresistance to cisplatin. Mechanistically, we found that the effects of the overexpression of COL11A1 in NSCLC cells were mediated by Smad signaling. Collectively, our findings suggest that COL11A1 may sever as a biomarker for metastatic NSCLC, and can be used to predict recurrence after surgical resection. Therapeutic approaches targeting COL11A1 may facilitate the optimization of cisplatin treatment of NSCLC by overcoming chemoresistance. IntroductionLung cancer is the most common type of cancer, and is the leading cause of human cancer-related deaths (1,2). Non-small cell lung carcinoma (NSCLC) accounts for approximately 85% of all cases of human lung cancer, including all types of epithelial lung cancer except small cell lung carcinoma (SCLC) (3). Generally, the 5-year survival rate of lung cancer patients is approximately 15% (2). For patients with different stages of lung cancer, the 5-year relative survival rate varies dramatically from 49 to 2% (2,4). However, approximately 70% of patients with lung cancer were found to present with intrathoracic or extrathoracic metastasis at initial diagnosis (3,5). Thus, it is crucial to detect lung cancer at an early stage, and to suppress the spread of primary cancer.Currently, surgical resection remains the single most successful treatment for patients with early-stage NSCLC (6,7). However, despite optimal surgical treatment, approximately half of the patients with NSCLC develop recurrence and succumb to the disease, even though they present with histologically negative lymph nodes (8,9). While bone is the most common target of distant metastasis from lung cancer, recurrent NSCLC is often systemic (4,8). Although the mechanisms of recurrent NSCLC remain unclear, several molecules have been reported to predict the recurrence of NSCLC. These include EphA2 (EPH receptor A2) receptor tyrosine kinase, USP17 and DNA methylation markers (10-12).The collagen type XI α1 (COL11A1) gene encodes one of the two α chains of type XI collagen, a minor fibrillar collagen (13). As a major component of the extracellular matrix (ECM), collagens are involved in the regulation of multiple biological processes, including cell proliferation, differentiation and migration (14,15). Type XI collagen is a heterotrimer, ...

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Collagen type XI α1 facilitates head and neck squamous cell cancer growth and invasion

Cited by 51 publications

References 31 publications

Tumor matrix protein collagen XIα1 in cancer

Tumor matrix protein collagen XIα1 in cancer

miR-15b regulates cisplatin resistance and metastasis by targeting PEBP4 in human lung adenocarcinoma cells

COL11A1 is overexpressed in recurrent non-small cell lung cancer and promotes cell proliferation, migration, invasion and drug resistance

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