RESUMO
Recent studies demonstrated that long non-coding RNAs (lncRNAs) have a critical role in the regulation of cancer progression and metastasis. However, little is known whether lncRNA regulated nasopharyngeal carcinoma (NPC) cell radioresistance. In the present study, we found that MALAT1 was significantly upregulated in NPC cell lines and tissues. Knockdown of MALAT1 could sensitize NPC cells to radiation both in vitro and in vivo. Interestingly, we found that MALAT1 regulated radioresistance by modulating cancer stem cell (CSC) activity. Furthermore, we found that there was reciprocal repression between MALAT1 and miR-1, and slug was identified as a downstream target of miR-1. Taking these observations into consideration, we proposed that MALAT1 regulated CSC activity and radioresistance by modulating miR-1/slug axis, which indicated that MALAT1 could act as a therapeutic target for NPC patients.
Assuntos
MicroRNAs/fisiologia , Neoplasias Nasofaríngeas/metabolismo , RNA Longo não Codificante/fisiologia , Fatores de Transcrição da Família Snail/fisiologia , Animais , Sequência de Bases , Sítios de Ligação , Linhagem Celular Tumoral , Feminino , Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Humanos , Estimativa de Kaplan-Meier , Masculino , Camundongos Nus , Pessoa de Meia-Idade , Neoplasias Nasofaríngeas/genética , Neoplasias Nasofaríngeas/mortalidade , Neoplasias Nasofaríngeas/radioterapia , Transplante de Neoplasias , Interferência de RNA , Tolerância a RadiaçãoRESUMO
Recent studies demonstrated that long noncoding RNAs (lncRNAs) have a critical role in the regulation of cancer progression and metastasis. However, little is known about the mechanism through which metastasis-associated lung adencarcinoma transcript 1 (MALAT1) exerts its oncogenic activity, and the interaction between MALAT1 and microRNA remains largely unknown. In the present study, we reported that MALAT1 was upregulated in triple-negative breast cancer (TNBC) tissues. Knockdown of MALAT1 inhibited proliferation, motility, and increased apoptosis in vitro. In vivo study indicated that knockdown of MALAT1 inhibited tumor growth and metastasis. Patients with high MALAT1 expression had poorer overall survival time than those with low MALAT1 expression. In addition, our findings demonstrate a reciprocal negative control relationship between MALAT1 and miR-1: downregulation of MALAT1 increased expression of microRNA-1 (miR-1), while overexpression of miR-1 decreased MALAT1 expression. Slug was identified as a direct target of miR-1. We proposed that MALAT1 exerted its function through the miR-1/slug axis. In summary, we proposed that MALAT1 may be a target for TNBC therapy.
Assuntos
Regulação Neoplásica da Expressão Gênica , MicroRNAs/genética , Proteínas de Neoplasias/fisiologia , RNA Longo não Codificante/genética , RNA Neoplásico/genética , Fatores de Transcrição da Família Snail/fisiologia , Neoplasias de Mama Triplo Negativas/genética , Regiões 3' não Traduzidas/genética , Animais , Linhagem Celular Tumoral , DNA Recombinante/genética , Feminino , Humanos , Estimativa de Kaplan-Meier , Camundongos Endogâmicos BALB C , Camundongos Nus , MicroRNAs/biossíntese , Pessoa de Meia-Idade , Invasividade Neoplásica , Proteínas de Neoplasias/biossíntese , Proteínas de Neoplasias/genética , RNA/genética , Interferência de RNA , RNA Longo não Codificante/biossíntese , RNA Neoplásico/biossíntese , RNA Interferente Pequeno/genética , Fatores de Transcrição da Família Snail/biossíntese , Fatores de Transcrição da Família Snail/genética , Organismos Livres de Patógenos Específicos , Neoplasias de Mama Triplo Negativas/metabolismo , Neoplasias de Mama Triplo Negativas/mortalidade , Neoplasias de Mama Triplo Negativas/patologiaRESUMO
OBJECTIVE: To study the effect of chemotherapy assisted with shenqi fuzheng injection (SFI) on senile patients with non-small cell lung cancer (NSCLC). METHODS: One hundred and twenty old patients with NSCLC were treated with NP chemotherapeutic protocol, to the 60 patients in the treated group among them, additional medication of SFI was started one week before the beginning of chemotherapy. The short-term therapeutic efficacy, long-term survival rate, changes on quality of life (QOL) and immune function of patients, and hematological toxicity of therapy were observed. RESULTS: Difference between the two groups on short-term therapeutic effect, 1- and 2-year survival rate showed no significance (P>0.05), but the 3-year survival rate in the treated group was 26.6%, while that in the control group was 11.7%, showed that the former was higher than the latter. After treatment QOL of the treated group was better than that of the control (P<0.05). Besides, the hematological toxicity and affection on immune function of chemotherapy after treatment in the treated group were all lower than those in the control group showing significant difference (P<0.05). CONCLUSION: SFI has definite toxicity relieving effect on chemotherapy in treating senile NSCLC.
