Novel functions of TIMPs in cell signaling

Chirco, Rosemarie; Liu, Xu Wen; Jung, Kyoung Hwa; Kim, Hyeong Reh Choi

doi:10.1007/s10555-006-7893-x

Cited by 367 publications

(350 citation statements)

References 166 publications

Supporting

Mentioning

332

Contrasting

Unclassified

Order By: Relevance

“…33 Oprin is a metalloproteinase inhibitor, which in some properties, but not in sequence, resembles the tissue inhibitor of metalloproteinases (TIMPs), a family of proteins with complex roles in tumor progression and angiogenesis. 34 An association of A1BG expression with cancer has been described in one previous study. In a study that utilized expressed sequence tag (EST) profiling of cDNA libraries, Yoon et al identified A1BG as 1 of 14 genes confirmed to be highly expressed in human hepatocellular carcinoma (HCC) cell lines and liver tumor tissue specimens.…”

Section: Discussionmentioning

confidence: 68%

“…Haptoglobin was also associated with bladder cancer in this study, and this glycoprotein has been reported to be diagnostically useful in both ovarian and liver cancer. 34,35 Further studies are needed in large cohorts of bladder cancer patients with a broad range of disease stage and grade and with noncancer conditions to evaluate the true potential of the glycoproteins implicated in this study in bladder disease management. Beyond the investigation of individual proteins identified here, the described technical approach will facilitate a more focused analysis of clinically relevant samples, such as urine and other bodily fluids, which in turn will lead to the identification of reliable biomarkers for improved detection, surveillance, and screening regimens for a range of diseases.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Bladder Cancer Associated Glycoprotein Signatures Revealed by Urinary Proteomic Profiling

et al. 2007

View full text Add to dashboard Cite

Current methods in the noninvasive detection and surveillance of bladder cancer via urine analysis include voided urine cytology (VUC) and some diagnostic urinary protein biomarkers; however, due to the poor sensitivity of VUC and high false-positive rates of currently available protein assays, detection of bladder cancer via urinalysis remains a challenge. In the study presented here, a rapid, high-sensitivity technique was developed to profile the N-linked glycoprotein component in naturally micturated human urine specimens. Concanavalin A (Con A) affinity chromatography coupled to nanoflow liquid chromatography was utilized to separate the complex peptide mixture prior to a linear ion trap MS analysis. Of 186 proteins identified with high confidence by multiple analyses, 40% were secreted proteins, 18% membrane proteins, and 14% extracellular proteins. In this study, the presence of several proteins appeared to be associated with the presence of bladder cancer, including R-1B-glycoprotein that was detected in all tumor-bearing patient samples but in none of the samples obtained from nontumor-bearing individuals. The combination of Con A affinity chromatography and nano-LC/MS/MS provides an initial investigation of N-glycoproteins in complex biological samples and facilitates the identification of potential biomarkers of bladder cancer in noninvasively obtained human urine.

show abstract

Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Bladder Cancer Associated Glycoprotein Signatures Revealed by Urinary Proteomic Profiling

et al. 2007

View full text Add to dashboard Cite

show abstract

“…During normal physiological conditions, the expression of MMPs is finely controlled and their activities are regulated by tissue inhibitors of metalloproteinases (TIMPs). However, when the balance between MMPs and TIMPs is disrupted, overexpression of MMPs will result in numerous pathogenic processes, including tumor invasion and metastasis (39,40). Overexpression of MMPs observed in most of human cancer cells and high levels of MMPs are linked to metastasis (12).…”

Section: Curcumin Suppresses the Expression Of Matrix Metalloproteinamentioning

confidence: 99%

Molecular Mechanisms of Anti-metastatic Activity of Curcumin

Deng

Verron

Rohanizadeh

2016

View full text Add to dashboard Cite

Abstract. Cancer is the leading cause of death worldwide. Although cancer occurs as a localized disease, its morbidity and mortality rates remain high due to the ability of cancer cells to break-off from the primary tumor and spread to distant organs. Currently, chemotherapy is the main treatment for cancer; however, the increase in proportion of drug-resistant cancer cells and unpleasant side-effects of chemotherapy are still the major challenges in cancer therapy. Curcumin is a natural polyphenol compound and the main bioactive constituent of Indian spice turmeric, widely used in Indian and Chinese medicines. Curcumin has well-known therapeutic actions, including antiinflammatory, anti-microbial, anti-oxidant and anti-cancer properties. Curcumin induces cancer cell apoptosis through regulating various signaling pathways and arresting tumor cell cycle. Curcumin's therapeutic/ preventative actions on metastatic cancers have not been yet fully understood and studied. The present review explores the potential anti-metastatic mechanisms of curcumin, including inhibition of transcription factors and their signaling pathways (e.g., inflammatory cytokines (e.g., CXCL1, CXCL2, multiple proteases (e.g., uPA, MMPs), multiple protein kinases (e.g., MAPKs, FAK), regulation of miRNAs (e.g., miR21, miR181b) and heat shock proteins (HLJ1). In addition, possible synergistic actions of combination therapy of curcumin with current chemotherapies are discussed in this review.Despite all recent advances in oncology, cancer is still one of the deadliest diseases around the world (1). Cancer occurs as a localized disease but can spread to distant organs through migration, invasion and metastasis (2). Metastatic cancer is one of the major causes of death in cancer patients. Metastasis is a complex process involving multiple steps: (i) local migration through degrading basement membrane and extracellular matrix (ECM), (ii) intravasation into blood and/or lymphatic vessels, (iii) circulating to the target organ site, (iv) extravasation into target organ tissue and, finally, (v) multiplication in the target organ (2, 3). These steps are mediated by various factors, including growth factors, proteolysis degradation of extracellular matrix, cell-cell adhesion, cytoskeleton remodeling and changes of genes' expressions (2, 3). Metastasis is a non-random process that means each metastatic cancer type has its own preferred site of metastasis. For example, breast cancer cells preferentially metastasize to regional lymph nodes, liver, lungs and bone (4). Nowadays, there are different therapeutic approaches available for patients with metastatic cancers, including surgery, radiotherapy and chemotherapy. Chemotherapy remains the main treatment modality for cancer patients because of its ability of preventing invasion and metastasis. However, the morbidity and mortality rates in patients with metastatic cancer still remain high since current chemotherapy agents fail to selectively and effectively kill cancer cells without destroying normal ce...

show abstract

“…A recent clinical study reports increases in fibronectin gene expression by alveolar macrophages and epithelial lining fluid recovered from alcohol abusing individuals (Burnham et al, 2007). ECM turnover is regulated by endogenous neutral endopeptidases in the lung, amongst which are the Zinc (Zn) dependent MMPs and TIMPs: the balance between MMPs and TIMPs determines either tissue homeostasis or disease state (Chirco et al, 2006;Greenlee et al, 2007;Murphy and Nagase, 2008). Recent studies suggest that pathogens can bind to ECM molecules via adhesins and use the ECM for survival and dissemination.…”

Section: Alcohol Modulates Immune Response During Bacterial and Viralmentioning

confidence: 99%

Alcohol, Signaling, and ECM Turnover

Seth

El-Guindy

Apte

et al. 2009

Alcoholism Clin & Exp Res

View full text Add to dashboard Cite

Alcohol is recognized as a direct hepatotoxin, but the precise molecular pathways that are important for the initiation and progression of alcohol-induced tissue injury are not completely understood. The current understanding of alcohol toxicity to organs suggests that alcohol initiates injury by generation of oxidative and nonoxidative ethanol metabolites and via translocation of gut-derived endotoxin. These processes lead to cellular injury and stimulation of the inflammatory responses mediated through a variety of molecules. With continuing alcohol abuse, the injury progresses through impairment of tissue regeneration and extracellular matrix (ECM) turnover, leading to fibrogenesis and cirrhosis. Several cell types are involved in this process, the predominant being stellate cells, macrophages, and parenchymal cells. In response to alcohol, growth factors and cytokines activate many signaling cascades that regulate fibrogenesis. This mini-review brings together research focusing on the underlying mechanisms of alcohol-mediated injury in a number of organs. It highlights the various processes and molecules that are likely involved in inflammation, immune modulation, susceptibility to infection, ECM turnover and fibrogenesis in the liver, pancreas, and lung triggered by alcohol abuse.

show abstract

Novel functions of TIMPs in cell signaling

Cited by 367 publications

References 166 publications

Bladder Cancer Associated Glycoprotein Signatures Revealed by Urinary Proteomic Profiling

Bladder Cancer Associated Glycoprotein Signatures Revealed by Urinary Proteomic Profiling

Molecular Mechanisms of Anti-metastatic Activity of Curcumin

Alcohol, Signaling, and ECM Turnover

Contact Info

Product

Resources

About