For TPM3 transcript quantification, the primer and probe set also recognized the low molecular weight isoforms 2 to 5. The liver cancer cells and clinical samples showed low/undetectable transcript levels of TPM3 high molecular weight isoform 1. Therefore, GEP should be associated with TPM3 low molecular weight isoforms in liver cancer. However, the association of GEP with TPM3 high molecular weight isoform in other cancer types could not be excluded because these isoforms have significant conserved sequences. Increased or decreased expression of different tropomyosin isoforms have also been reported in a number of human solid tumors, although the functional significance of differential expression is unclear. In the present study, we have demonstrated elevated expression of TPM3 in HCC. Dysregulation of TPM3 has also been reported in other human diseases. Missense mutation in the TPM3 has been reported to be associated with autosomal nemaline myopathy, a disease characterized by the presence of muscle fibres in the pathognomonic rod bodies. In anaplastic large-cell lymphoma, TPM3 is involved in hematopoietic tumorigenesis by forming TPM3-ALK fusion through chromosome translocation. TPM3-ALK fusion gene is further investigated to be involved in transformation, proliferation, invasion and metastasis in anaplastic large-cell lymphoma. Notably, chromosomal gain at 1q, 8q and 17q are frequently detected in HCC. These chromosomal regions may contain important oncogenes or growth factors. TPM3 is located at the region of chromosome 1q21.2. In a recent study examining the HCC genetic aberrations using whole-genome array-CGH, TPM3 has been identified in the recurrent gain region on chromosome 1q as important for HCC tumorigenesis. Therefore, overexpression of TPM3 would potentially be explained by gene amplification rather than mutation or gene fusion mechanism. In summary, we are the first group to demonstrate that TPM3 is a predominant interacting partner of GEP in the cytoplasm of HCC cells. Notably, TPM3 has been reported to control migration, invasion and anchorage-independent growth of HCC cells, and previously we have reported that GEP regulates growth, invasion and anchorage-independent growth of HCC cells. As the current study demonstrated TPM3 as the WZ8040 cytoplasmic interacting partner of GEP, thus the two molecules may act together to control the invasion and anchorage-independent growth ability of the HCC cells. Further studies to investigate other TPM family members with GEP on their potential proteinprotein interactions would be warranted. Allergic airway inflammation and airway hyperresponsiveness are characteristics of atopic asthma pathophysiology. More than 7% of Americans suffer from asthma, and annual expenditure for health and lost productivity due to asthma is estimated at nearly $20 billion. The currently available therapeutic approaches for asthma usually include quick symptomatic relief measures directed to relaxation of airway smooth muscle and long-term control with suppression of airway inflammation.