Limits...
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-╬▒and IL-1╬▓. 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-╬▒ and IL-1╬▓, 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-╬▒ and IL-1╬▓. 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 transcription of TNF-╬▒and IL-1╬▓in Hela and C33A cells. (A,B) STAT3 over expression increased TNF-╬▒transcription in Hela cells (A) and C33A cells (B). (C,D) STAT3 over expression increased IL-1╬▓transcription in Hela cells (C) and C33A cells (D). NC: normal control. STAT3: STAT3 up regulation group. IL37-NC: IL-37 gene transfection groups. IL37+STAT3: IL-37 and STAT3 gene transfection group.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4543756&req=5

Figure 6: STAT3 up regulation restored the transcription of TNF-╬▒and IL-1╬▓in Hela and C33A cells. (A,B) STAT3 over expression increased TNF-╬▒transcription in Hela cells (A) and C33A cells (B). (C,D) STAT3 over expression increased IL-1╬▓transcription in Hela cells (C) and C33A cells (D). NC: normal control. STAT3: STAT3 up regulation group. IL37-NC: IL-37 gene transfection groups. IL37+STAT3: IL-37 and STAT3 gene transfection group.

Mentions: STAT3 up regulation restored the transcription of TNF-╬▒and IL-1╬▓. Compared IL37-NC group to IL37+STAT3 group, STAT3 over expression increased TNF-╬▒ transcription level from 0.43 to 0.95 (relative to GAPDH) in Hela cells (Figure 6A) and from 0.55 to 0.89 (relative to GAPDH) in C33A cells (Figure 6B). Compared IL37-NC group to IL37+STAT3 group, STAT3 over expression increased IL-1╬▓transcription level from 0.42 to 0.92 (relative to GAPDH) in Hela cells (Figure 6C) and from 0.49 to 0.93 (relative to GAPDH) in C33A cells (Figure 6D).


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 transcription of TNF-╬▒and IL-1╬▓in Hela and C33A cells. (A,B) STAT3 over expression increased TNF-╬▒transcription in Hela cells (A) and C33A cells (B). (C,D) STAT3 over expression increased IL-1╬▓transcription in Hela cells (C) and C33A cells (D). NC: normal control. STAT3: STAT3 up regulation group. IL37-NC: IL-37 gene transfection groups. IL37+STAT3: IL-37 and STAT3 gene transfection group.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4543756&req=5

Figure 6: STAT3 up regulation restored the transcription of TNF-╬▒and IL-1╬▓in Hela and C33A cells. (A,B) STAT3 over expression increased TNF-╬▒transcription in Hela cells (A) and C33A cells (B). (C,D) STAT3 over expression increased IL-1╬▓transcription in Hela cells (C) and C33A cells (D). NC: normal control. STAT3: STAT3 up regulation group. IL37-NC: IL-37 gene transfection groups. IL37+STAT3: IL-37 and STAT3 gene transfection group.
Mentions: STAT3 up regulation restored the transcription of TNF-╬▒and IL-1╬▓. Compared IL37-NC group to IL37+STAT3 group, STAT3 over expression increased TNF-╬▒ transcription level from 0.43 to 0.95 (relative to GAPDH) in Hela cells (Figure 6A) and from 0.55 to 0.89 (relative to GAPDH) in C33A cells (Figure 6B). Compared IL37-NC group to IL37+STAT3 group, STAT3 over expression increased IL-1╬▓transcription level from 0.42 to 0.92 (relative to GAPDH) in Hela cells (Figure 6C) and from 0.49 to 0.93 (relative to GAPDH) in C33A cells (Figure 6D).

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-╬▒and IL-1╬▓. 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-╬▒ and IL-1╬▓, 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-╬▒ and IL-1╬▓. 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