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Long noncoding RNA CCAT2 promotes breast tumor growth by regulating the Wnt signaling pathway.

Cai Y, He J, Zhang D - Onco Targets Ther (2015)

Bottom Line: In addition to protein-coding genes, the human genome makes a large amount of noncoding RNAs, including microRNAs and long noncoding RNAs (lncRNAs).Also, the biological function of CCAT2 was explored and the results showed silencing of CCAT2 could suppress cell growth in vitro and tumor formation in vivo.Finally, our results revealed that the abnormal expression of CCAT2 could influence the Wnt signaling pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Geriatric Oncology, The General Hospital of Chinese People's Liberation Army, Beijing City, People's Republic of China.

ABSTRACT
In addition to protein-coding genes, the human genome makes a large amount of noncoding RNAs, including microRNAs and long noncoding RNAs (lncRNAs). Emerging evidence indicates that lncRNAs could have a critical role in the regulation of cellular processes such as cell growth and apoptosis as well as cancer progression and metastasis. The lncRNA CCAT2 is dysregulated in several cancers such as colon cancer, non-small cell lung cancer, esophageal squamous cell carcinoma, gastric cancer, and breast cancer; however, the contributions of CCAT2 to breast cancer remain largely unknown. In the current paper, we first confirmed the high expression level of CCAT2 in breast cancer tissues and breast cancer cell lines by reverse transcription quantitative polymerase chain reaction (RT-qPCR) assay, and we further analyzed the relationship between CCAT2 expression and clinical prognostic factors. Also, the biological function of CCAT2 was explored and the results showed silencing of CCAT2 could suppress cell growth in vitro and tumor formation in vivo. Finally, our results revealed that the abnormal expression of CCAT2 could influence the Wnt signaling pathway. In conclusion, lncRNA CCAT2 might be considered as a novel molecule involved in breast cancer development, which provides a potential therapeutic target for breast cancer.

No MeSH data available.


Related in: MedlinePlus

Suppressing CCAT2 expression decreases cell proliferation and invasion in vitro.Notes: (A) The transfection efficiency of si-CCAT2 in MCF-7 and MDA-MB-231 cells were indicated by RT-qPCR compared with cells transfected with si-NS. (B) An MTT assay was performed to investigate the effects of si-CCAT2 on cell proliferation in MCF-7 and MDA-MB-231 cells. The data showed that si-CCAT2 inhibited the cell growth of breast cancer cells. (C) A transwell assay was performed to investigate the effects of si-CCAT2 on cell invasion in MCF-7 and MDA-MB-231 cells. The data showed si-CCAT2 inhibited the invasion of breast cancer cells. The experiments were all repeated at least three times. *P<0.05 vs the control.Abbreviations: RT-qPCR, reverse transcription quantitative polymerase chain reaction; h, hour(s); si-CCAT2, siRNA specifically targeting CCAT2; si-NS, nonspecific siRNA; si-NS, scram bled nucleotide used as the negative control.
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f3-ott-8-2657: Suppressing CCAT2 expression decreases cell proliferation and invasion in vitro.Notes: (A) The transfection efficiency of si-CCAT2 in MCF-7 and MDA-MB-231 cells were indicated by RT-qPCR compared with cells transfected with si-NS. (B) An MTT assay was performed to investigate the effects of si-CCAT2 on cell proliferation in MCF-7 and MDA-MB-231 cells. The data showed that si-CCAT2 inhibited the cell growth of breast cancer cells. (C) A transwell assay was performed to investigate the effects of si-CCAT2 on cell invasion in MCF-7 and MDA-MB-231 cells. The data showed si-CCAT2 inhibited the invasion of breast cancer cells. The experiments were all repeated at least three times. *P<0.05 vs the control.Abbreviations: RT-qPCR, reverse transcription quantitative polymerase chain reaction; h, hour(s); si-CCAT2, siRNA specifically targeting CCAT2; si-NS, nonspecific siRNA; si-NS, scram bled nucleotide used as the negative control.

Mentions: To further investigate the role of CCAT2 in human breast cancer cells, si-CCAT2 was designed and transfected into MCF-7 and MDA-MB-231 breast cancer cells. Nonspecific siRNA (si-NS) was used as the negative control. As shown in Figure 3A, cells transfected with si-CCAT2 presented a significantly decreased mRNA expression level of CCAT2 compared with the si-NS group in both cells (P<0.05) (Figure 3A). The MTT assay showed that the proliferation rate was downregulated in the si-CCAT2-transfected breast cancer cells after 48 hours compared with the si-NS group (P<0.05) (Figure 3B). Furthermore, to analyze the role of CCAT2 in cell invasion, transwell assays were performed in MCF-7 and MDA-MB-231 cells, and the result indicated that the invasiveness of both the MCF-7 and MDA-MB-231 cells transfected with si-CCAT2 were greatly decreased compared with the si-NS groups, respectively (Figure 3C). All together, the data demonstrated that suppression of CCAT2 expression could inhibit cell proliferation and invasion of breast cancer cells in vitro.


Long noncoding RNA CCAT2 promotes breast tumor growth by regulating the Wnt signaling pathway.

Cai Y, He J, Zhang D - Onco Targets Ther (2015)

Suppressing CCAT2 expression decreases cell proliferation and invasion in vitro.Notes: (A) The transfection efficiency of si-CCAT2 in MCF-7 and MDA-MB-231 cells were indicated by RT-qPCR compared with cells transfected with si-NS. (B) An MTT assay was performed to investigate the effects of si-CCAT2 on cell proliferation in MCF-7 and MDA-MB-231 cells. The data showed that si-CCAT2 inhibited the cell growth of breast cancer cells. (C) A transwell assay was performed to investigate the effects of si-CCAT2 on cell invasion in MCF-7 and MDA-MB-231 cells. The data showed si-CCAT2 inhibited the invasion of breast cancer cells. The experiments were all repeated at least three times. *P<0.05 vs the control.Abbreviations: RT-qPCR, reverse transcription quantitative polymerase chain reaction; h, hour(s); si-CCAT2, siRNA specifically targeting CCAT2; si-NS, nonspecific siRNA; si-NS, scram bled nucleotide used as the negative control.
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Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4590572&req=5

f3-ott-8-2657: Suppressing CCAT2 expression decreases cell proliferation and invasion in vitro.Notes: (A) The transfection efficiency of si-CCAT2 in MCF-7 and MDA-MB-231 cells were indicated by RT-qPCR compared with cells transfected with si-NS. (B) An MTT assay was performed to investigate the effects of si-CCAT2 on cell proliferation in MCF-7 and MDA-MB-231 cells. The data showed that si-CCAT2 inhibited the cell growth of breast cancer cells. (C) A transwell assay was performed to investigate the effects of si-CCAT2 on cell invasion in MCF-7 and MDA-MB-231 cells. The data showed si-CCAT2 inhibited the invasion of breast cancer cells. The experiments were all repeated at least three times. *P<0.05 vs the control.Abbreviations: RT-qPCR, reverse transcription quantitative polymerase chain reaction; h, hour(s); si-CCAT2, siRNA specifically targeting CCAT2; si-NS, nonspecific siRNA; si-NS, scram bled nucleotide used as the negative control.
Mentions: To further investigate the role of CCAT2 in human breast cancer cells, si-CCAT2 was designed and transfected into MCF-7 and MDA-MB-231 breast cancer cells. Nonspecific siRNA (si-NS) was used as the negative control. As shown in Figure 3A, cells transfected with si-CCAT2 presented a significantly decreased mRNA expression level of CCAT2 compared with the si-NS group in both cells (P<0.05) (Figure 3A). The MTT assay showed that the proliferation rate was downregulated in the si-CCAT2-transfected breast cancer cells after 48 hours compared with the si-NS group (P<0.05) (Figure 3B). Furthermore, to analyze the role of CCAT2 in cell invasion, transwell assays were performed in MCF-7 and MDA-MB-231 cells, and the result indicated that the invasiveness of both the MCF-7 and MDA-MB-231 cells transfected with si-CCAT2 were greatly decreased compared with the si-NS groups, respectively (Figure 3C). All together, the data demonstrated that suppression of CCAT2 expression could inhibit cell proliferation and invasion of breast cancer cells in vitro.

Bottom Line: In addition to protein-coding genes, the human genome makes a large amount of noncoding RNAs, including microRNAs and long noncoding RNAs (lncRNAs).Also, the biological function of CCAT2 was explored and the results showed silencing of CCAT2 could suppress cell growth in vitro and tumor formation in vivo.Finally, our results revealed that the abnormal expression of CCAT2 could influence the Wnt signaling pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Geriatric Oncology, The General Hospital of Chinese People's Liberation Army, Beijing City, People's Republic of China.

ABSTRACT
In addition to protein-coding genes, the human genome makes a large amount of noncoding RNAs, including microRNAs and long noncoding RNAs (lncRNAs). Emerging evidence indicates that lncRNAs could have a critical role in the regulation of cellular processes such as cell growth and apoptosis as well as cancer progression and metastasis. The lncRNA CCAT2 is dysregulated in several cancers such as colon cancer, non-small cell lung cancer, esophageal squamous cell carcinoma, gastric cancer, and breast cancer; however, the contributions of CCAT2 to breast cancer remain largely unknown. In the current paper, we first confirmed the high expression level of CCAT2 in breast cancer tissues and breast cancer cell lines by reverse transcription quantitative polymerase chain reaction (RT-qPCR) assay, and we further analyzed the relationship between CCAT2 expression and clinical prognostic factors. Also, the biological function of CCAT2 was explored and the results showed silencing of CCAT2 could suppress cell growth in vitro and tumor formation in vivo. Finally, our results revealed that the abnormal expression of CCAT2 could influence the Wnt signaling pathway. In conclusion, lncRNA CCAT2 might be considered as a novel molecule involved in breast cancer development, which provides a potential therapeutic target for breast cancer.

No MeSH data available.


Related in: MedlinePlus