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Interleukin 37 Expression Inhibits STAT3 to Suppress the Proliferation and Invasion of Human Cervical Cancer Cells.

Wang S, An W, Yao Y, Chen R, Zheng X, Yang W, Zhao Y, Hu X, Jiang E, Bie Y, Chen Z, Ouyang P, Zhang H, Xiong H - J Cancer (2015)

Bottom Line: Firstly, we found that IL-37 inhibited STAT3 expression at both mRNA and protein levels.Secondly, blockage of STAT3 using siRNAs reduced significantly the ability of IL-37 to suppress cell proliferation and invasion.This study demonstrated a new biological function of IL-37 and offered a potential molecule for CC treatment.

View Article: PubMed Central - PubMed

Affiliation: 1. Cancer Institute, Guangdong Medical University, Dongguan 523808, China;

ABSTRACT

Objectives: The most recently discovered cytokine interleukin 37 (IL-37) received growing attention. Its function on tumor is largely unknown. Here, we investigated the biological function of IL-37 on cervical cancer (CC). Materials and methods : HPV(+) Hela cells and HPV(-) C33A cells were used. RT-qPCR was performed to detect the transcription of IL-37, STAT3, TNF-αand IL-1β. Western blotting was used for protein detection. CCK-8 assay and transwell assay were employed for cell proliferation and invasion detection, respectively. Results : Successful gene transfection of IL-37 suppressed the proliferation and invasion of CC. Interestingly, IL-37 showed higher anticancer ability in HPV(+) Hela cells than that in HPV(-) C33A cells. Then, the molecular mechanism of IL-37 anticancer was explored. Firstly, we found that IL-37 inhibited STAT3 expression at both mRNA and protein levels. IL-37 also down regulated the phosphorylation of STAT3. Secondly, blockage of STAT3 using siRNAs reduced significantly the ability of IL-37 to suppress cell proliferation and invasion. Thirdly, STAT3 knockdown reduced markedly the inhibition of IL-37 on the transcription of tumor-derived TNF-α and IL-1β, indicating the contribution of STAT3 for the cancer associated antiinflammation of IL-37. Finally, STAT3 up regulation restored the ability of cell proliferation, cell invasion and the expression of inflammatory cytokines, TNF-α and IL-1β. Conclusions : IL-37 suppressed cell proliferation and invasion of CC and STAT3 is involved in this process. Thus, IL-37 emerges as a new anticancer cytokine for CC. This study demonstrated a new biological function of IL-37 and offered a potential molecule for CC treatment.

No MeSH data available.


Related in: MedlinePlus

STAT3 up regulation restored the proliferation and invasion ability in Hela and C33A cells. (A, B) STAT3 gene transfection increased the mRNA expression of STAT3 in Hela (A) and C33A (B) cells. (C, D) STAT3 gene transfection increased the protein expression of STAT3 in Hela (C) and C33A (D) cells. (E, F) STAT3 increased the cell proliferation ability Hela (E) and C33A (F) cells. (G, H) STAT3 increased the cell invasion of Hela (G) and C33A (H) cells. (I, J) STAT3 transfection decreased the inhibition rate of proliferation and restored the cell proliferation in Hela (I) and C33A (J) cells. (K, L) STAT3 transfection decreased the inhibition rate of invasion and restored the cell invasion of Hela (K) and C33A (L) cells. NC: normal control. STAT3: STAT3 up regulation group. IL37-NC: IL-37 gene transfection group. IL37+STAT3: STAT3 and IL-37 gene transfection group.
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Figure 5: STAT3 up regulation restored the proliferation and invasion ability in Hela and C33A cells. (A, B) STAT3 gene transfection increased the mRNA expression of STAT3 in Hela (A) and C33A (B) cells. (C, D) STAT3 gene transfection increased the protein expression of STAT3 in Hela (C) and C33A (D) cells. (E, F) STAT3 increased the cell proliferation ability Hela (E) and C33A (F) cells. (G, H) STAT3 increased the cell invasion of Hela (G) and C33A (H) cells. (I, J) STAT3 transfection decreased the inhibition rate of proliferation and restored the cell proliferation in Hela (I) and C33A (J) cells. (K, L) STAT3 transfection decreased the inhibition rate of invasion and restored the cell invasion of Hela (K) and C33A (L) cells. NC: normal control. STAT3: STAT3 up regulation group. IL37-NC: IL-37 gene transfection group. IL37+STAT3: STAT3 and IL-37 gene transfection group.

Mentions: Transfection of STAT3 expression vector successfully up regulated STAT3 expression. The mRNA level of STAT3 increased by 98% in Hela cells (Figure 5A) and 110% in C33A cells (Figure 5B). The protein level of STAT3 increased by 90.71% in Hela cells (Figure 5C) and 66.08% in C33A cells (Figure 5D), respectively. Figure 5E and 5F showed that STAT3 gene transfection restored the cell proliferation. Figure 3G and 3H showed that STAT3 gene transfection restored the cell invasion.


Interleukin 37 Expression Inhibits STAT3 to Suppress the Proliferation and Invasion of Human Cervical Cancer Cells.

Wang S, An W, Yao Y, Chen R, Zheng X, Yang W, Zhao Y, Hu X, Jiang E, Bie Y, Chen Z, Ouyang P, Zhang H, Xiong H - J Cancer (2015)

STAT3 up regulation restored the proliferation and invasion ability in Hela and C33A cells. (A, B) STAT3 gene transfection increased the mRNA expression of STAT3 in Hela (A) and C33A (B) cells. (C, D) STAT3 gene transfection increased the protein expression of STAT3 in Hela (C) and C33A (D) cells. (E, F) STAT3 increased the cell proliferation ability Hela (E) and C33A (F) cells. (G, H) STAT3 increased the cell invasion of Hela (G) and C33A (H) cells. (I, J) STAT3 transfection decreased the inhibition rate of proliferation and restored the cell proliferation in Hela (I) and C33A (J) cells. (K, L) STAT3 transfection decreased the inhibition rate of invasion and restored the cell invasion of Hela (K) and C33A (L) cells. NC: normal control. STAT3: STAT3 up regulation group. IL37-NC: IL-37 gene transfection group. IL37+STAT3: STAT3 and IL-37 gene transfection group.
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Related In: Results  -  Collection

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Figure 5: STAT3 up regulation restored the proliferation and invasion ability in Hela and C33A cells. (A, B) STAT3 gene transfection increased the mRNA expression of STAT3 in Hela (A) and C33A (B) cells. (C, D) STAT3 gene transfection increased the protein expression of STAT3 in Hela (C) and C33A (D) cells. (E, F) STAT3 increased the cell proliferation ability Hela (E) and C33A (F) cells. (G, H) STAT3 increased the cell invasion of Hela (G) and C33A (H) cells. (I, J) STAT3 transfection decreased the inhibition rate of proliferation and restored the cell proliferation in Hela (I) and C33A (J) cells. (K, L) STAT3 transfection decreased the inhibition rate of invasion and restored the cell invasion of Hela (K) and C33A (L) cells. NC: normal control. STAT3: STAT3 up regulation group. IL37-NC: IL-37 gene transfection group. IL37+STAT3: STAT3 and IL-37 gene transfection group.
Mentions: Transfection of STAT3 expression vector successfully up regulated STAT3 expression. The mRNA level of STAT3 increased by 98% in Hela cells (Figure 5A) and 110% in C33A cells (Figure 5B). The protein level of STAT3 increased by 90.71% in Hela cells (Figure 5C) and 66.08% in C33A cells (Figure 5D), respectively. Figure 5E and 5F showed that STAT3 gene transfection restored the cell proliferation. Figure 3G and 3H showed that STAT3 gene transfection restored the cell invasion.

Bottom Line: Firstly, we found that IL-37 inhibited STAT3 expression at both mRNA and protein levels.Secondly, blockage of STAT3 using siRNAs reduced significantly the ability of IL-37 to suppress cell proliferation and invasion.This study demonstrated a new biological function of IL-37 and offered a potential molecule for CC treatment.

View Article: PubMed Central - PubMed

Affiliation: 1. Cancer Institute, Guangdong Medical University, Dongguan 523808, China;

ABSTRACT

Objectives: The most recently discovered cytokine interleukin 37 (IL-37) received growing attention. Its function on tumor is largely unknown. Here, we investigated the biological function of IL-37 on cervical cancer (CC). Materials and methods : HPV(+) Hela cells and HPV(-) C33A cells were used. RT-qPCR was performed to detect the transcription of IL-37, STAT3, TNF-αand IL-1β. Western blotting was used for protein detection. CCK-8 assay and transwell assay were employed for cell proliferation and invasion detection, respectively. Results : Successful gene transfection of IL-37 suppressed the proliferation and invasion of CC. Interestingly, IL-37 showed higher anticancer ability in HPV(+) Hela cells than that in HPV(-) C33A cells. Then, the molecular mechanism of IL-37 anticancer was explored. Firstly, we found that IL-37 inhibited STAT3 expression at both mRNA and protein levels. IL-37 also down regulated the phosphorylation of STAT3. Secondly, blockage of STAT3 using siRNAs reduced significantly the ability of IL-37 to suppress cell proliferation and invasion. Thirdly, STAT3 knockdown reduced markedly the inhibition of IL-37 on the transcription of tumor-derived TNF-α and IL-1β, indicating the contribution of STAT3 for the cancer associated antiinflammation of IL-37. Finally, STAT3 up regulation restored the ability of cell proliferation, cell invasion and the expression of inflammatory cytokines, TNF-α and IL-1β. Conclusions : IL-37 suppressed cell proliferation and invasion of CC and STAT3 is involved in this process. Thus, IL-37 emerges as a new anticancer cytokine for CC. This study demonstrated a new biological function of IL-37 and offered a potential molecule for CC treatment.

No MeSH data available.


Related in: MedlinePlus