Tumorigenicity of BALB3T3 A31 cells transfected with hamster‐complement‐C1s cDNA

Sakai, Norie; Kusunoki, Mayumi; Nishida, Munehiro; Toyoguchi, Toru; Fukutomi, Hisayuki; Sakiyama, Hisako

doi:10.1002/ijc.2910580227

Cited by 8 publications

(6 citation statements)

References 27 publications

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“…MMP11, also known as stromelysin 3, is significantly linked to the lymph node involvement of nonsmallcell lung cancer [32]. C1S confers tumorigenicity to hamster fibroblasts [33], possibly in coordination with MMP9, a type IV collagenase [34]. In contrast, our present observations have demonstrated that several collagen genes, COL1A1, 6A1, and 3A1, are abundantly expressed in advanced OSCC tissues.…”

Section: Discussioncontrasting

confidence: 74%

Gene expression signatures that classify the mode of invasion of primary oral squamous cell carcinomas

Kondoh

Ishikawa

Ohkura

et al. 2008

Molecular Carcinogenesis

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To identify molecular signatures and establish a new diagnostic model for progressive oral squamous cell carcinoma (OSCC). Total RNAs were isolated from primary OSCCs from both node-positive and -negative patients and used in cDNA microarray analysis. To identify marker genes representing a malignant phenotype, their expression was further examined by quantitative reverse transcription-PCR (QRT-PCR) in 64 OSCC tissues. Using Fisher's linear discriminant analysis (LDA) fitted with a stepwise increment method, we created discriminatory predictor models. The stability of these models was examined using leave-one-out cross validation. Immunohistochemical analysis was performed. Among the 16,600 possible target cDNAs in the array analysis, 83 genes demonstrated significantly differential signals (>2-fold). We further identified 53 marker genes that can be implicated in the Yamamoto-Kohama's (YKs) mode of invasion for OSCCs (P < 0.06). Using LDA fitted with a stepwise increment method, we created four discriminatory predictor models based on 16- to 25-gene signatures which could best distinguish the five established grades of YKs mode of invasion. Leave-one out validation demonstrated that the stability of these models was 92-95%. For validation, we also examined an independent set of 13 primary OSCCs; the predictor models determined the invasion status from 77% to 100% (on average, 85%) fidelity with the pathological observations. TGM3 protein expression was markedly suppressed in highly invasive OSCCs. We reveal novel gene expression alterations during the progression of OSCC, and have constructed prediction models for the evaluation of the invasion status of these cancers.

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Section: Discussioncontrasting

confidence: 74%

Gene expression signatures that classify the mode of invasion of primary oral squamous cell carcinomas

Kondoh

Ishikawa

Ohkura

et al. 2008

Molecular Carcinogenesis

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“…reported that when hamster complement C1s cDNA was transfected into BALB/c mouse fibroblast A31 cells, the transfectants formed tumors in BALB/c-nu/nu mice. 29 In a subsequent study, the same authors transfected mutant C1s cDNA into A31 cells. However, the transfectants, which produced C1S without enzyme activity, did not form tumors in nude mice.…”

Section: Discussionmentioning

confidence: 99%

Complement Component 1, s Subcomponent Overexpression is an Independent Poor Prognostic Indicator in Patients with Urothelial Carcinomas of the Upper Urinary Tract and Urinary Bladder

Chang

Lin

et al. 2016

J. Cancer

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Purpose: Urothelial carcinoma of the urinary bladder and upper tract is prevalent. By subjecting a documented transcriptome data set of urothelial carcinoma of bladder (GSE31684) to data mining and focusing on genes linked to peptidase activity (GO:0008233), we recognized C1S as the most significantly upregulated gene related to an advanced tumor status and metastasis. We subsequently analyzed the association of both C1S mRNA and its encoded protein expression with the clinical and pathological significance.Materials and Methods: We used real-time reverse transcription polymerase chain reaction to detect C1S transcription levels in 20 cases each of urothelial carcinoma of bladder and upper tract. An immunohistochemical stain was conducted to determine C1s protein expression levels in patients with urothelial carcinoma of upper tract (n = 340) and urinary bladder (n = 295). Furthermore, we examined the correlation of C1s expression with clinicopathological characteristics, disease-specific survival, and metastasis-free survival.Results: C1S transcription levels were significantly high in patients with advanced-stage tumors of both groups (all P < .05). Immunohistochemical analysis revealed that C1s expression levels were significantly associated with adverse clinicopathological parameters in both groups of urothelial carcinoma (all P < .05). C1s overexpression predicted poor disease-specific and metastasis-free survival rates for both urothelial carcinoma groups in the univariate analysis, and it was also an independent prognostic factor in the multivariate analysis (all P < .05).Conclusions: C1s may play a pivotal role in urothelial carcinoma progress and can represent a vital prognostic marker and a promising new therapeutic target in urothelial carcinoma.

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“…Non-canonical functions of the complement proteins: Many complement components, such as C1q, C1s, C3, properdin, FH, FI, etc have non-canonical, extracellular and intracellular functions, modulating the fundamental processes of the tumor cell in selected models, promoting proliferation and tumor progression when tested in animal models 44,[60][61][62] . In embryonic development and in cancer models, intracellular C3 impacts epithelial to mesenchymal transition 52 .…”

Section: Direct Impact Of Complement Effectors On Tumor Cell Biologymentioning

confidence: 99%

Context-dependent roles of complement in cancer

et al. 2019

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The tumor microenvironment (TME) highly influences the growth, spreading of tumors and therefore patient's clinical outcome. In this context, complement system plays a major and complex role. It may either kill antibody-coated tumor cells or support local inflammation, hamper anti-tumor T cell responses favoring cancer spreading. Recent studies demonstrate that these opposite effects depend of the sites of its activation, the composition of the TME and the tumor cell sensitivity to complement attack. In this review, we present the implication of complement activation and its effects on cancer control and clinical outcome in different TME contexts. We also provide an overview of the publicly available transcriptomic data on the prognostic value of complement genes expression in 30 cancer types. We argue that the interplay of complement within each cancer is unique, governed by the properties of the tumor cells and the TME. This concept is of critical importance for the design of efficient therapeutic strategies.

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Tumorigenicity of BALB3T3 A31 cells transfected with hamster‐complement‐C1s cDNA

Cited by 8 publications

References 27 publications

Gene expression signatures that classify the mode of invasion of primary oral squamous cell carcinomas

Gene expression signatures that classify the mode of invasion of primary oral squamous cell carcinomas

Complement Component 1, s Subcomponent Overexpression is an Independent Poor Prognostic Indicator in Patients with Urothelial Carcinomas of the Upper Urinary Tract and Urinary Bladder

Context-dependent roles of complement in cancer

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