ArticleTranslational cancer research2020
Silencing of DHX32 increases the proliferation of liver cancer cells.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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1 citing paper in PubMed, 2 citations in OpenAlex.
- Erratum to silencing of DHX32 increases the proliferation of liver cancer cells.Translational cancer research · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLiver cancer ranks fifth in malignancy incidence globally and is the second leading cause of cancer-related death in China. Chronic hepatitis B or C infection and alcohol abuse have been identified to be the major risk factors for liver cancer development. Some evidence implicates DHX32 as being critically involved in tumor progression. The role of DHX32 in liver cancer specifically, however, remains unclear.
methodsFifty-three liver cancer tissue and paracancerous tissue samples were surgically resected from 53 patients who were admitted to Zhongshan Hospital between 2006 and 2008. We used immunohistochemistry (IHC) to analyze the expressions of DHX32, established liver cancer cells with stable DHX32 knockdown, and investigated the proliferation of these cells with methyl thiazolyl tetrazolium (MTT) and 5-ethynyl-2'-deoxyuridine (EdU) data.
resultBaseline characteristics of enrolled liver cancer patients (53 patients) were summarized, and the IHC results firstly showed that 88.7% (47/53) of paracancerous tissues exhibited a high expression of DHX32, while only 43.4% (23/53) of liver cancer tissues showed similar expression. We then established liver cancer cells with the stable knockdown of DHX32. MTT and EdU data demonstrated that DHX32 knockdown in liver cancer cells enhanced the proliferative potential of liver cancer cells. Furthermore, phosphorylated levels of extracellular signal-regulated kinase (ERK) and protein kinase B (Akt) were upregulated in liver cancer cells with DHX32 knockdown. We also found the level of cyclin-dependent kinases 6 (CDK6) to be increased in liver cancer cells with DHX32 knockdown.
conclusionsDHX32 showed a lower expression in liver cancer tissues than in paracancerous tissues and could harbor a proliferation-suppressing property in liver cancer. DHX32 may thus be a possible target for gene therapy.
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