LncRNA ZFPM2-AS1 aggravates the malignant development of breast cancer via upregulating JMJD6.

OBJECTIVE: The purpose of this study was to explore the expression pattern of long non-coding RNA (lncRNA) ZFPM2-AS1 in breast cancer (BC) tissues, and its biological influence on clinical features and prognosis in BC patients. PATIENTS AND METHODS: ZFPM2-AS1 levels in 52 paired BC tissues and adjacent normal ones were detected. Then, the relationship between ZFPM2-AS1 level and clinical features in BC patients was analyzed. Regulatory effects of ZFPM2-AS1 on proliferative and migratory abilities in MCF-7 and SKBR3 cells were assessed. In addition, in vivo regulation of ZFPM2-AS1 in nude mice bearing BC was evaluated. Finally, the interaction between ZFPM2-AS1 and JMJD6 and the involvement of ZFPM2-AS1 in the development of BC were illustrated. RESULTS: The results showed that ZFPM2-AS1 was upregulated in BC tissues, and its high level was linked to advanced tumor stage, high rates of lymphatic metastasis, and distant metastasis, as well as poor prognosis in BC. The knockdown of ZFPM2-AS1 suppressed proliferative and migratory abilities in BC cells. In addition, JMJD6 was verified to be the downstream gene binding to ZFPM2-AS1, which was highly expressed in BC tissues and positively regulated by ZFPM2-AS1. In vivo knockdown of ZFPM2-AS1 in nude mice bearing BC showed a smaller tumor volume and lower tumor weight than controls. In addition, JMJD6 was downregulated in BC tumors extracted from mice with silenced ZFPM2-AS1. CONCLUSIONS: LncRNA ZFPM2-AS1 is upregulated in BC and linked to tumor stage, metastasis, and prognosis in BC patients. It aggravates the malignant development of BC via upregulating JMJD6.

[Chromosome aberration and carcinogenicity of CHO dhfr- cells transformed by plasmid containing S+ and Pre S1 of fusion gene of hepatitis B virus].

OBJECTIVE: To investigate the chromosome aberrations and carcinogenicity of CHO-dhfr- cell induced by integration of plasmid containing S+ and Pre S1 fusion gene of hepatitis B surface antigen (HBsAg). METHODS: The plasmid pCHBSS1G was constructed with S+ Pre S1 of HBsAg. CHO-dhfr- cells were transformed with this recombinant plasmid DNA and CHO cells lines with integrated DNA were cloned and named GdSS118. The GdSS1 18 cell lines secreting the S+ Pre S1 fusion protein of HBsAg at high level were developed by screening in increased concentration of MTX and MSX in cultured media. To make sample of cells chromosome, the cells integrated DNA were subcutaneously injected into nude mouse. RESULTS: The CHO-dhfr- cell lines integrated with S and Pre S1 fusion protein of HBsAg were developed and named GdSS1-18 cell lines. The frequencies and type of chromosome aberrations of the GdSS1-18 cell lines with different passage generations were 11%, 56% and 29%, respectively, while that of the control CHO-dhfr- cell lines was 6%. There was no change in the mode of chromosomes, both cell lines having 20 chromosome s. Both cell lines were non-oncogenic in nude mouse. CONCLUSIONS: The chromosome aberration of CHO-dhfr- cells with integrated DNA were obviously higher than that of the original CHO-dhfr- cells without integrated DNA. Both cell lines were non oncogenic in nude mouse.

Etiologic and serologic investigations of the 1980 epidemic of dengue fever on Hainan Island, China.

Virologic and seroepidemiologic studies were carried out during an epidemic of dengue fever on Hainan Island in 1980. Dengue 3 virus was isolated from 46 of 77 acute phase sera and from 1 of 10 pools of adult Aedes aegypti. Dengue 1 virus virus was isolated from a single acute phase serum. Seroepidemiologic investigations showed that 74% of healthy individuals in the epidemic area had antibody to dengue virus compared to 54% in an area where epidemic dengue had occurred in 1978, and less than or equal to 8% in nonepidemic areas. There were no significant differences in antibody prevalence for different sex and age groups.