TM may be a modulator of cancer metastasis in HCC. Downregulation of TM expression may increase ZEB1 and decrease E-cadherin levels.

Background: Hepatocellular carcinoma (HCC) is a worldwide health problem. Currently, there is no effective clinical therapeutic strategy for HCC. Smoking is associated with several malignant diseases including cancers. Experimental approach: However, the impact of smoking on HCC is still unresolved. Retrospectively reviewed HCC patients diagnosed between 1 January 2010 and 31 December 2015 at Taipei Medical University-Shuang Ho Hospital (Ministry of Health and Welfare). We found that smoking was associated with a poor prognosis, especially recurrence and patient survival after curative surgery using a clinicopathological analysis. Results: Our univariate and multivariate analyses showed that the α7-nicotinic acetylcholine receptor (α7-nAChR) was an oncogene and risk factor for post-resection recurrence. The α7-nAChR was overexpressed in HCC tissues compared to their non-tumor counterparts. Silencing the α7-nAChR reduced the viability of HCC cells, suppressed cellular proliferation, attenuated migration and invasion, and diminished the tumor’s sphere-formation ability, with concurrent downregulation of expression levels of the TGR5, p-JAK2, p-STAT3 (Tyr705/Ser727), RhoA, ROCK1, MMP2, and MMP9 proteins. Furthermore, a positive correlation was found between α7-nAChR and JAK2 expressions (p = 0.01) in HCC specimens, as well as their membranous co-localization. Conclusion: Together, we demonstrated that the α7-nAChR may be an independent prognosticator of the progression and prognosis of HCC patients. These findings suggest that the α7-nAChR drives the progression and recurrence of HCC through JAK2/STAT3 signaling and is a novel target for anti-HCC therapy.

Background Colorectal cancer (CRC) is the third most common cancer in the world. Genome‐wide association studies are a powerful method to analyze the status of single‐nucleotide polymorphisms (SNPs) in specific genes. Heat shock proteins (HSPs) were found to be involved in the cancer progression and chemoresistance. However, there is still no further study about polymorphisms of HSP beta‐1 (HSPB1) in colorectal cancer. We proposed the SNP of HSPB1 may be correlated with the progression and metastasis in colon cancer. Methods We recruited 379 colorectal cancer patients and categorized as four stages following the UICC TNM system. Then, we selected tagging SNPs of HSPB1 by 10% minimum allelic frequency in Han Chinese population from the HapMap database and analyze with the Chi‐square test. Results We demonstrated the association of HSPB1 genetic polymorphisms rs2070804 with tumor depth with colorectal cancer. But, there is a lack of association between HSPB1 genetic polymorphisms and colorectal cancer invasion, recurrence or metastasis. Conclusions The polymorphisms of HSPB1 seemed to change the tumor behavior of colorectal cancer. HSPB1 rs2070804 polymorphism is associated with the depth of the primary tumor. But, there is no further correlation with other to the clinical parameters such as cancer invasiveness, local recurrence, or distant metastasis.