Efficacy and Potential MicroRNA Mechanism for Computed Tomography-Guided Percutaneous Radiofrequency Ablation of Primary Lung Cancer and Lung Metastasis from Liver Cancer

Abstract

Background: The aim of this study was to evaluate comparatively the effectiveness of computed tomography-guided percutaneous radiofrequency ablation (CT-PRFA) for primary non-small cell lung cancer (NSCLC) and lung metastases from hepatocellular carcinoma (HCC) and to explore the potential miRNA mechanisms for the efficacy of CT-PRFA. Methods: 14 patients pathologically diagnosed with NSCLC and 12 patients with lung metastases from HCC were enrolled in the study and underwent CT-PRFA. Clinical outcomes were compiled on the basis of review of medical records, imaging follow-up reports, and any biopsy-proved residual or recurrent disease. Real-time RT-PCR was used to quantify the selected miRNAs known to be play key roles in lung cancer. Results: A total of 21 tumors were treated with umbrella-tip electrodes and spiral-tip electrodes were used for the remaining 8 tumors. The median follow-up was 13.5 months (range, 3-30 months) and no patient was lost to follow-up. The rate of technique efficacy for primary tumors was ∼93% (13 of 14). Treatment was successful in 11 out of 12 (91.7%) lung metastases patients. Overall survival rate was 80.8% at 2 years, and cancer-specific survival rate was 100% at 2 years. The tumor-free survival was 69.2% at 1 year and 26.9% at 2 years. Before PRFA, tumor suppressor let-7a and miR-34a were downregulated whereas oncomiR miR-21 was upregulated in primary tumors, and let-7a and miR-126 levels were downregulated whereas oncomiRs miR-21, miR-155 and miR-17-5p/miR-20b levels were upregulated in secondary tumors. This abnormal expression was normalized by CT-PRFA. Most notably, CT-PRFA failed to normalize the deregulated miRNAs in the non-survivors. Conclusions: CT-PRFA is a effective treatment for primary NSCLCs and secondary lung tumors from HCC and the efficacy may be related to its ability to normalize deregulated expression of miRNAs: upregulating tumor suppressor miRNAs and downregulating oncomiRs.

Role of MiR-3619-5p in β-Catenin-Mediated Non-Small Cell Lung Cancer Growth and Invasion

“…Non-small cell lung cancer (NSCLC) is a prevalent cancer and contains three subtypes: squamous cell carcinoma, large cell carcinoma, and adenocarcinoma [1][2][3][4]. NSCLCs are often insensitive to chemotherapy and radiotherapy, and are fast-growing and highly invasive [3][4][5][6][7][8][9][10].…”

“…NSCLCs are often insensitive to chemotherapy and radiotherapy, and are fast-growing and highly invasive [3][4][5][6][7][8][9][10]. Thus, understanding of the mechanisms underlying the growth and invasion of NSCLC are extremely important for its therapy.…”

Serum miR-335 Level is Associated with the Treatment Response to Trans-Arterial Chemoembolization and Prognosis in Patients with Hepatocellular Carcinoma

“…MiR-127 post-transcriptionally suppresses cell growth in hepatocellular carcinoma cells [11]. Abnormal expression of a series of miRNA, including miR-21, miR-155 and miR-17-5p/miR-20b, is observed in primary lung cancer and secondary lung tumors from HCC, which can be normalized by percutaneous radiofrequency ablation [12].…”

“…Recently, the role of miRNAs in tumorgenesis and metastasis has attracted increasing interest [11][12][13]. Specifically, miR-335 has been shown to act as a suppressor of tumor metastasis by regulating several classic signal pathways [14][15][16].…”

A Function Variant at miR-501 Alters Susceptibility to Hepatocellular Carcinoma in a Chinese Han Population

“…Among these, miRNA was found to regulate negatively post-transcriptional gene expression by cleaving target mRNA or by inhibiting their translation [14][15][16]. For example, miR-145 acts as a tumor suppressor and its downregulation in tumor tissues may contribute to the progression and metastasis of HCC through a mechanism involving ROCK1, suggesting that miR-145 is a potential new diagnostic and therapeutic target for the treatment of HCC [17].…”