Literature DB >> 25493224

Tumour suppressor HLJ1: A potential diagnostic, preventive and therapeutic target in non-small cell lung cancer.

Meng-Feng Tsai1, Chi-Chung Wang1, Jeremy Jw Chen1.   

Abstract

Lung cancer is the leading cause of cancer-related mortality throughout the world. Non-small cell lung cancer (NSCLC) accounts for 85% of all diagnosed lung cancers. Despite considerable progress in the diagnosis and treatment of the disease, the overall 5-year survival rate of NSCLC patients remains lower than 15%. The most common causes of death in lung cancer patients are treatment failure and metastasis. Therefore, developing novel strategies that target both tumour growth and metastasis is an important and urgent mission for the next generation of anticancer therapy research. Heat shock proteins (HSPs), which are involved in the fundamental defence mechanism for maintaining cellular viability, are markedly activated during environmental or pathogenic stress. HSPs facilitate rapid cell division, metastasis, and the evasion of apoptosis in cancer development. These proteins are essential players in the development of cancer and are prime therapeutic targets. In this review, we focus on the current understanding of the molecular mechanisms responsible for HLJ1's role in lung cancer carcinogenesis and progression. HLJ1, a member of the human HSP 40 family, has been characterised as a tumour suppressor. Research studies have also reported that HLJ1 shows promising dual anticancer effects, inhibiting both tumour growth and metastasis in NSCLC. The accumulated evidence suggests that HLJ1 is a potential biomarker and treatment target for NSCLC.

Entities:  

Keywords:  Anticancer; Biomarker; HLJ1; Metastasis; Non-small cell lung cancer

Year:  2014        PMID: 25493224      PMCID: PMC4259948          DOI: 10.5306/wjco.v5.i5.865

Source DB:  PubMed          Journal:  World J Clin Oncol        ISSN: 2218-4333


  95 in total

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Review 7.  Heat Shock Proteins and HSF1 in Cancer.

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8.  Clinical implications of transforming growth factor-beta-induced gene-h3 protein expression in lung cancer.

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