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MiR-195 suppresses non-small cell lung cancer by targeting CHEK1.

Liu B, Qu J, Xu F, Guo Y, Wang Y, Yu H, Qian B - Oncotarget (2015)

Bottom Line: Our previous study showed high miR-195 plasma levels associated with favorable overall survival of non-smoking women with lung adenocarcinoma.We demonstrated that miR-195 expression was lower in tumor tissues and was associated with poor survival outcome.High expression of CHEK1 in lung tumors was associated with poor overall survival.

View Article: PubMed Central - PubMed

Affiliation: Department of Epidemiology and Biostatistics, Key Laboratory of Breast Cancer Prevention and Therapy, Ministry of Education, Key Laboratory of Cancer Prevention and Therapy, Tianjin, National Clinical Research Center of Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.

ABSTRACT
MiR-195 suppresses tumor growth and is associated with better survival outcomes in several malignancies including non-small cell lung cancer (NSCLC). Our previous study showed high miR-195 plasma levels associated with favorable overall survival of non-smoking women with lung adenocarcinoma. To further elucidate role of miR-195 in NSCLC, we conducted in vitro experiment as well as clinical studies in a cohort of 299 NSCLC samples. We demonstrated that miR-195 expression was lower in tumor tissues and was associated with poor survival outcome. Overexpression of miR-195 suppressed tumor cell growth, migration and invasion. We discovered that CHEK1 was a direct target of miR-195, which decreased CHEK1 expression in lung cancer cells. High expression of CHEK1 in lung tumors was associated with poor overall survival. Our results suggest that miR-195 suppresses NSCLC and predicts lung cancer prognosis.

No MeSH data available.


Related in: MedlinePlus

MiR-195 expression, cell proliferation and cell-cycle arrest in lung cancer cellsIncreasing miR-195 expression in lung cancer cell lines reduced cell proliferation and induced cell-cycle arrest. Cell lines A549 (A), H1299 (B) and H1975 (C) were transfected with miR-195 or miR-NC, and cell proliferation was measured by the MTT assay. Cell-cycle analysis was performed by flow cytometer to determine the impact of miR-195 or miR-NC on cell-cycle progression. The representative flow cytometry patterns in 3 cell lines were shown in (D) and the G1/S and G2/S ratios in each cell line were shown in (E) (n = 3).
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Figure 2: MiR-195 expression, cell proliferation and cell-cycle arrest in lung cancer cellsIncreasing miR-195 expression in lung cancer cell lines reduced cell proliferation and induced cell-cycle arrest. Cell lines A549 (A), H1299 (B) and H1975 (C) were transfected with miR-195 or miR-NC, and cell proliferation was measured by the MTT assay. Cell-cycle analysis was performed by flow cytometer to determine the impact of miR-195 or miR-NC on cell-cycle progression. The representative flow cytometry patterns in 3 cell lines were shown in (D) and the G1/S and G2/S ratios in each cell line were shown in (E) (n = 3).

Mentions: After transfecting lung cancer cells (A549, H1299 and H1975) with miR-195 mimic or scrambled miRNA control (miR-NC), we quantified cell numbers with the MTT assay. The results showed that compared to the miRNA control, the number of viable cells was clearly reduced overtime in all 3 cell lines transfected with miR-195 mimic (p < 0.05) (Figure 2A, 2B and 2C), suggesting that cell proliferation was significantly suppressed by miR-195. Furthermore, using flow cytometry to assess cell-cycle status, we found that cells transfected with miR-195 had increased cell numbers in the G1 and G2 phases, but reduced numbers in the S phase (Figure 2D). Analysis of the G1/S and G2/S ratios suggested that miR-195-related cell-cycle arrest occurred both in the G1 and G2 checkpoints for A549 and H1299, but only in G2 for H1975 (Figure 2E).


MiR-195 suppresses non-small cell lung cancer by targeting CHEK1.

Liu B, Qu J, Xu F, Guo Y, Wang Y, Yu H, Qian B - Oncotarget (2015)

MiR-195 expression, cell proliferation and cell-cycle arrest in lung cancer cellsIncreasing miR-195 expression in lung cancer cell lines reduced cell proliferation and induced cell-cycle arrest. Cell lines A549 (A), H1299 (B) and H1975 (C) were transfected with miR-195 or miR-NC, and cell proliferation was measured by the MTT assay. Cell-cycle analysis was performed by flow cytometer to determine the impact of miR-195 or miR-NC on cell-cycle progression. The representative flow cytometry patterns in 3 cell lines were shown in (D) and the G1/S and G2/S ratios in each cell line were shown in (E) (n = 3).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4496229&req=5

Figure 2: MiR-195 expression, cell proliferation and cell-cycle arrest in lung cancer cellsIncreasing miR-195 expression in lung cancer cell lines reduced cell proliferation and induced cell-cycle arrest. Cell lines A549 (A), H1299 (B) and H1975 (C) were transfected with miR-195 or miR-NC, and cell proliferation was measured by the MTT assay. Cell-cycle analysis was performed by flow cytometer to determine the impact of miR-195 or miR-NC on cell-cycle progression. The representative flow cytometry patterns in 3 cell lines were shown in (D) and the G1/S and G2/S ratios in each cell line were shown in (E) (n = 3).
Mentions: After transfecting lung cancer cells (A549, H1299 and H1975) with miR-195 mimic or scrambled miRNA control (miR-NC), we quantified cell numbers with the MTT assay. The results showed that compared to the miRNA control, the number of viable cells was clearly reduced overtime in all 3 cell lines transfected with miR-195 mimic (p < 0.05) (Figure 2A, 2B and 2C), suggesting that cell proliferation was significantly suppressed by miR-195. Furthermore, using flow cytometry to assess cell-cycle status, we found that cells transfected with miR-195 had increased cell numbers in the G1 and G2 phases, but reduced numbers in the S phase (Figure 2D). Analysis of the G1/S and G2/S ratios suggested that miR-195-related cell-cycle arrest occurred both in the G1 and G2 checkpoints for A549 and H1299, but only in G2 for H1975 (Figure 2E).

Bottom Line: Our previous study showed high miR-195 plasma levels associated with favorable overall survival of non-smoking women with lung adenocarcinoma.We demonstrated that miR-195 expression was lower in tumor tissues and was associated with poor survival outcome.High expression of CHEK1 in lung tumors was associated with poor overall survival.

View Article: PubMed Central - PubMed

Affiliation: Department of Epidemiology and Biostatistics, Key Laboratory of Breast Cancer Prevention and Therapy, Ministry of Education, Key Laboratory of Cancer Prevention and Therapy, Tianjin, National Clinical Research Center of Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.

ABSTRACT
MiR-195 suppresses tumor growth and is associated with better survival outcomes in several malignancies including non-small cell lung cancer (NSCLC). Our previous study showed high miR-195 plasma levels associated with favorable overall survival of non-smoking women with lung adenocarcinoma. To further elucidate role of miR-195 in NSCLC, we conducted in vitro experiment as well as clinical studies in a cohort of 299 NSCLC samples. We demonstrated that miR-195 expression was lower in tumor tissues and was associated with poor survival outcome. Overexpression of miR-195 suppressed tumor cell growth, migration and invasion. We discovered that CHEK1 was a direct target of miR-195, which decreased CHEK1 expression in lung cancer cells. High expression of CHEK1 in lung tumors was associated with poor overall survival. Our results suggest that miR-195 suppresses NSCLC and predicts lung cancer prognosis.

No MeSH data available.


Related in: MedlinePlus