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Research article

CX3CR1 regulates hepatocellular carcinoma(HCC) metastasis via PI3K/AKT pathway

Mengtian Fan, Yaguang Weng, Xian Li, Yingjiu Jiang, Xiaowen Wang, Mengjun Bie, Liqin An, Qiong Shi
DOI: 10.21203/rs.2.12811/v1

Abstract

Background

Fractalkine receptor CX3CR1 is differentially expressed in hepatocellular carcinoma and its function is unknown. As a special case of chemokine family, CX3CR1 only binds to its unique ligand CX3CL1, and CX3CL1 also only binds to its only receptor CX3CR1, the unique matching between ligands and receptors is not found in other chemokines, and this specificity is essential for diagnosis, prognosis and clinical target therapy.

Methods

CX3CR1 expression was analyzed by immunohistochemistry, migration and invasion abilities of SMMC-7721 cells were detected by wound-healing and transwell after overexpressing CX3CR1. In addition to overexpression experiments, interfering RNA siCX3CR1 was used for reverse validation in HepG2 cells. To further clarify the mechanism of CX3CR1 regulating HCC metastasis, the classical PI3K/AKT pathway were detected by Western blot.

Results

The CX3CR1 levels were positive correlated with pathological TNM stage, meanwhile a negative correlation between high expression of CX3CR1 and survival rate was found among patients at stageII-III. In our study, overexpression of CX3CR1 promoted migration and invasion ability of SMMC-7721 cells, whereas knockout of CX3CR1 inhibited these abilities of HepG2 cells. Mechanistically, CX3CR1 regulates the metastasis of HCC cells via PI3K/AKT pathway, and the PI3K inhibitor LY294002 could stop the promoting effect of CX3CR1 on SMMC-7721 cells.

Conclusion

CX3CR1 regulated HCC cell metastasis via PI3K/AKT signaling and this effect might be a new target for clinical diagnosis and treatment.

Keywords
Carcinoma; Hepatocellular; CX3CR1; Metastasis; AKT

Figures

Background

Methods

Results

Discussion

Conclusions

Abbreviations

References

Declarations

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Posted 14 Aug, 2019

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    Received 20 Aug, 2019

  • Reviewer #3 agreed

    On 09 Aug, 2019

  • Reviewer #2 agreed

    On 08 Aug, 2019

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    On 08 Aug, 2019

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  • Reviewer #1 agreed

    On 08 Aug, 2019

  • Submission checks complete

    On 07 Aug, 2019

  • Editor invited

    On 07 Aug, 2019

  • First submitted

    On 31 Jul, 2019

Subject Areas

Cancer Biology

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Preprint: Please note that this article has not completed peer review.
Research article

CX3CR1 regulates hepatocellular carcinoma(HCC) metastasis via PI3K/AKT pathway

Mengtian Fan, Yaguang Weng, Xian Li, Yingjiu Jiang, Xiaowen Wang, Mengjun Bie, Liqin An, Qiong Shi

STATUS: In Review

Comments: 0
PDF Downloads: 0
HTML Views: 1

Integrity Check:

  • Article

  • Peer Review Timeline

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Abstract

Background

Fractalkine receptor CX3CR1 is differentially expressed in hepatocellular carcinoma and its function is unknown. As a special case of chemokine family, CX3CR1 only binds to its unique ligand CX3CL1, and CX3CL1 also only binds to its only receptor CX3CR1, the unique matching between ligands and receptors is not found in other chemokines, and this specificity is essential for diagnosis, prognosis and clinical target therapy.

Methods

CX3CR1 expression was analyzed by immunohistochemistry, migration and invasion abilities of SMMC-7721 cells were detected by wound-healing and transwell after overexpressing CX3CR1. In addition to overexpression experiments, interfering RNA siCX3CR1 was used for reverse validation in HepG2 cells. To further clarify the mechanism of CX3CR1 regulating HCC metastasis, the classical PI3K/AKT pathway were detected by Western blot.

Results

The CX3CR1 levels were positive correlated with pathological TNM stage, meanwhile a negative correlation between high expression of CX3CR1 and survival rate was found among patients at stageII-III. In our study, overexpression of CX3CR1 promoted migration and invasion ability of SMMC-7721 cells, whereas knockout of CX3CR1 inhibited these abilities of HepG2 cells. Mechanistically, CX3CR1 regulates the metastasis of HCC cells via PI3K/AKT pathway, and the PI3K inhibitor LY294002 could stop the promoting effect of CX3CR1 on SMMC-7721 cells.

Conclusion

CX3CR1 regulated HCC cell metastasis via PI3K/AKT signaling and this effect might be a new target for clinical diagnosis and treatment.

Figures

Background

Methods

Results

Discussion

Conclusions

Abbreviations

References

Declarations

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