ABSTRACT
Objective To study the epidemiological characteristics of family cancer history in patients with nasopharyngeal carcinoma in Dongguan city. Methods A total of 240 patients with nasopharyngeal cancer treated in our hospital from January 2017 to January 2021 were selected for the investigation of family cancer history. The families of the patients were determined respectively, and the family cancer history of the first, second and third relatives was obtained. The incidence, population distribution and incidence factors were investigated and analyzed. Results A total of 7 918 primary, secondary and tertiary relatives of 240 cases were inquired. 188 cases were found to have cancer, including 118 cases of nasopharyngeal cancer and 70 cases of non-nasopharyngeal cancer (10 cases of digestive tract cancer, 18 cases of breast cancer, 20 cases of lymphoma and 22 cases of lung cancer). The incidence of familial cancer was higher in males (127/240) than in females (79/188). The main pathological type of family cancer was squamous cell carcinoma (109/188), accounting for 57.98%. Most of the patients in family cancer group were farmers (128/188), accounting for 68.09%; There was no significant difference in the prevalence of nasopharyngeal carcinoma and non-nasopharyngeal carcinoma in relatives of different genders (χ2=0.11, χ2=0.23, P>0.05). The incidence of cancer in first-degree relatives of different genders was higher than that in second-degree relatives, and the differences were statistically significant (χ2=4.26, χ2=5.62, P2 times per week), Epstein-Barr virus infection was significantly higher than that of the familial non-cancer group, the difference was statistically significant (χ2=6.57, χ2=10.59, P<0.05). Conclusions The incidence of cancer and nasopharyngeal cancer in first-degree relatives is significantly higher than that in second-level and third-level relatives. The occurrence of nasopharyngeal cancer is the result of the combined action of genetic factors and environmental factors. It is necessary to carry out health education for the families of nasopharyngeal cancer, Avoid eating and curing foods, and actively improve production and living environment, so as to reduce the incidence rate of nasopharyngeal carcinoma.
ABSTRACT
BACKGROUND: The incidence of nasopharyngeal carcinoma is increasing gradually, but the pathogenesis is not completely clear. MicroRNA, a highly conserved endogenous noncoding small molecule RNA, plays an essential role in the regulation of gene expression and is a hotspot in cancer research worldwide. OBJECTIVES: Although previous studies have confirmed that the abnormal expression of microRNAs is closely related to the progression of nasopharyngeal carcinoma, the role of miRNA-331-3p in nasopharyngeal carcinoma has not been studied. The purpose of this study was to explore the role and mechanism of miRNA-331-3p in the progression of nasopharyngeal carcinoma. MATERIALS AND METHODS: Real-time quantitative reverse transcription polymerase chain reaction was performed to detect the expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cell lines (CNE-1 and 5-8F cells). After overexpression of miRNA-331-3p in CNE-1 cells, cell proliferation was measured by Cell Counting Kit-8 assay, cell invasion was detected by Transwell assay, and apoptosis was tested by flow cytometry. In addition, the dual-luciferase reporter assay was used to identify the target gene of miRNA-331-3p and Western blotting was performed to measure the relative protein expression. RESULTS: The expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cells was decreased significantly. Overexpression of miRNA-331-3p markedly inhibited the proliferation and invasion of CNE-1 cells and promoted cell apoptosis. Moreover, overexpression of miRNA-331-3p reduced the expression of target gene elF4B, leading to inhibition of the phosphorylation of Phosphoinositide 3-kinase (PI3K) and Serine/ threonine kinase (AKT). CONCLUSION: miRNA-331-3p inhibited cell proliferation and induced cell apoptosis in nasopharyngeal carcinoma by targeting elF4B gene and then blocked the PI3K-AKT signaling pathway. SIGNIFICANCE: The role of miRNA-331-3p in the development of NPC and its mechanism provide new ideas for the treatment of nasopharyngeal carcinoma.
Subject(s)
Apoptosis , Cell Proliferation , Class I Phosphatidylinositol 3-Kinases/antagonists & inhibitors , Eukaryotic Initiation Factors/antagonists & inhibitors , MicroRNAs/genetics , Nasopharyngeal Carcinoma/pathology , Proto-Oncogene Proteins c-akt/antagonists & inhibitors , Cell Line, Tumor , Cell Movement , Class I Phosphatidylinositol 3-Kinases/metabolism , Eukaryotic Initiation Factors/metabolism , Gene Expression Regulation, Neoplastic , Humans , Nasopharyngeal Carcinoma/genetics , Nasopharyngeal Carcinoma/metabolism , Nasopharyngeal Neoplasms/genetics , Nasopharyngeal Neoplasms/metabolism , Nasopharyngeal Neoplasms/pathology , Proto-Oncogene Proteins c-akt/metabolism , Signal TransductionABSTRACT
<p><b>BACKGROUND AND OBJECTIVE</b>Sonodynamic therapy (SDT) is a promising new approach for cancer therapy. The purpose of this study is to detect the effects of SDT on the cell proliferation of human lung adenocarcinoma cell SPCA-1, using Chlorin e6 as a sonosensitizing agent activated by ultrasound.</p><p><b>METHODS</b>SPCA-1 and normal peripheral mononuclear cell (PMNC) were treated with ultrasound or Chlorin e6 alone and combined. Cell proliferation was determined by MTT assay, and cell morphology was studied by inverted microscope after 6 h treated.</p><p><b>RESULTS</b>1.0 MHz ultrasound (1.0 W/ cm(2)-2.0 W/cm2 x 60 s) and Chlorin e6 (0.4 mg/mL-3.2 mg/mL) inhibited the cell proliferation of both SPCA-1 and PMNC cells in a intensity- and a dose-dependent manner respectively. Compared with the ultrasound (1.0 W/cm2 x 60 s) or Chlorin e6 (0.05 mg/mL-0.2 mg/mL) alone, the inhibitory effect on the cell proliferation was remarkably increased by the combination of ultrasound and chlorin e6 in SPCA-1 cells (P < 0.05), but no same effect was observed in PMNC cells (P > 0.05). Compared with the ultrasound (1.0 W/cm2 x 60 s) or chlorin e6 (0.2 mg/mL) alone, the combination treatment of ultrasound with Chlorin e6 induced more necrotic cells in SPCA-1 cells (P < 0.05).</p><p><b>CONCLUSION</b>There was a significant selectively inhibitory effect of sonodynamic effect with Chlorin e6 on the SPCA-1 cell growth. Chlorin e6 may be a promising sonosensitizing agent for the treatment of non-small cell lung cancer.</p>
Subject(s)
Humans , Adenocarcinoma , Drug Therapy , Therapeutics , Cell Line, Tumor , Lung Neoplasms , Drug Therapy , Therapeutics , Porphyrins , Chemistry , Therapeutic Uses , Radiation-Sensitizing Agents , Chemistry , Therapeutic Uses , Ultrasonic Therapy , MethodsABSTRACT
Objective:To evaluate the sonodynamic effect of chlorin-e6, a sonosensitizing agent, on the proliferation of MDA-MB-231 cells. Methods:MDA-MB-231 and normal peripheral mononuclear cells (PMNCs) were treated with chlorin-e6 alone or combined with ultrasound. Cell proliferation was determined by MTT assay and cell morphology was observed under inversed fluorescence microscope. Results:Treatment with ultrasound (1.0 MHz, 1.0-2.0 W/cm~2,60 s) or chlorin-e6 (0.10-1.60 mg/mL) alone significantly inhibited the cell proliferation of both MDA-MB-231 and PMNC cells in a intensity-dependent and a dose-dependent manner, respectively. The 50% intensity of ultrasound for inhibiting the growth of MDA-MB-231 and PMNC cells was 1.23 W/cm~2 and 1.25 W/cm~2, respectively (P>0.05) and the IC_(50) of chlorin-e6 was 0.38 mg/mL and 0.77 mg/mL, respectively (P0.05). Compared with single ultrasound treatment (1.0 MHz, 0.5 W/cm~2,60 s) and single chlorin-e6 treatment (0.20 mg/mL), combination of ultrasound and chlorin-e6 significantly increased the death rate of MDA-MB-231 cells (P<0.05). Conclusion:Ultrasound combined with chlorin-e6 exerted specific inhibitory effect on the proliferation of MDA-MB-231 cells. Chlorin-e6 may be a promising sonosensitizing agent for the treatment of breast cancer.