Limits...
SNX16 negatively regulates the migration and tumorigenesis of MCF-7 cells.

Zhang L, Qin D, Hao C, Shu X, Pei D - Cell Regen (Lond) (2013)

Bottom Line: Ectopic expression of SNX16 reduces the migration and the tumor formation activity of MCF-7 cells.Our results indicate that, in addition to the PI3P, there is a SNX23- and microtubule-dependent cargo transport pathway required for the proper subcellular distribution of SNX16.SNX16 plays a negative regulatory role during cell migration and tumorigenesis.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Regenerative Biology, Chinese Academy of Sciences, and Guangdong Provincial Key Laboratory of Stem Cells and Regenerative Medicine, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Guangzhou, 510530 China.

ABSTRACT

Background: Sorting nexins are a large family of proteins that are associated with various components of the endosome system and they play many roles in processes such as endocytosis, intracellular protein trafficking and cell signaling. The subcellular distribution patterns of many of them remain controversial and their in vivo functions have not been characterized yet.

Results: We investigated the subcellular distribution and function of SNX16 in this study. SNX16 is detected on Rab5-positive endosomes localized adjacent to focal adhesions at cell cortex. Inhibition of SNX23, polymerization of microtubule filaments as well as the PI3-kinase all disrupt the cell cortex distribution of SNX16. Ectopic expression of SNX16 reduces the migration and the tumor formation activity of MCF-7 cells.

Conclusion: Our results indicate that, in addition to the PI3P, there is a SNX23- and microtubule-dependent cargo transport pathway required for the proper subcellular distribution of SNX16. SNX16 plays a negative regulatory role during cell migration and tumorigenesis.

No MeSH data available.


Related in: MedlinePlus

SNX16 negatively regulates tumorigenesis of MCF-7 cellsin vivo. (A) Stable MCF-7 cell lines expressing SNX16, SNX2 or the empty vector were injected subcutaneously into the SCID mice and the sizes of tumors formed at the indicated time (day) were determined. (B, C) Tumors were dissected and weighted 27 days post inoculation. Over-expression of SNX16 but not SNX2 reduces the tumorigenic activity of MCF-7 cells. Data represent mean ± SD from 7 mice (for Vector or SNX16) or 5 mice (for SNX2).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4230745&req=5

Fig4: SNX16 negatively regulates tumorigenesis of MCF-7 cellsin vivo. (A) Stable MCF-7 cell lines expressing SNX16, SNX2 or the empty vector were injected subcutaneously into the SCID mice and the sizes of tumors formed at the indicated time (day) were determined. (B, C) Tumors were dissected and weighted 27 days post inoculation. Over-expression of SNX16 but not SNX2 reduces the tumorigenic activity of MCF-7 cells. Data represent mean ± SD from 7 mice (for Vector or SNX16) or 5 mice (for SNX2).

Mentions: MCF-7 is a breast cancer derived cell line that can induce tumor formation when injected subcutaneously into the SCID mice. We investigated whether or not the ectopic expression of SNX16 has an effect on the tumorigenic activity of this cell line. Stable MCF-7 cell lines expressing the empty vector or SNX2 are used as the control. We injected these cells into the SCID mice, monitored the sizes of the tumors and finally determined the weights of tumors 27 days post inoculation after the dissection of tumors. We found that the ectopic expression of SNX16 but not SNX2 significantly reduces the tumor formation activity of MCF-7 cells (Figure 4, P=0.001, 0.0002 and 0.27 for SNX16-1, SNX16-2 and SNX2 respectively). Together, our results suggest that SNX16 is a negative regulator of cell migration and tumorigenesis in vivo.Figure 4


SNX16 negatively regulates the migration and tumorigenesis of MCF-7 cells.

Zhang L, Qin D, Hao C, Shu X, Pei D - Cell Regen (Lond) (2013)

SNX16 negatively regulates tumorigenesis of MCF-7 cellsin vivo. (A) Stable MCF-7 cell lines expressing SNX16, SNX2 or the empty vector were injected subcutaneously into the SCID mice and the sizes of tumors formed at the indicated time (day) were determined. (B, C) Tumors were dissected and weighted 27 days post inoculation. Over-expression of SNX16 but not SNX2 reduces the tumorigenic activity of MCF-7 cells. Data represent mean ± SD from 7 mice (for Vector or SNX16) or 5 mice (for SNX2).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4230745&req=5

Fig4: SNX16 negatively regulates tumorigenesis of MCF-7 cellsin vivo. (A) Stable MCF-7 cell lines expressing SNX16, SNX2 or the empty vector were injected subcutaneously into the SCID mice and the sizes of tumors formed at the indicated time (day) were determined. (B, C) Tumors were dissected and weighted 27 days post inoculation. Over-expression of SNX16 but not SNX2 reduces the tumorigenic activity of MCF-7 cells. Data represent mean ± SD from 7 mice (for Vector or SNX16) or 5 mice (for SNX2).
Mentions: MCF-7 is a breast cancer derived cell line that can induce tumor formation when injected subcutaneously into the SCID mice. We investigated whether or not the ectopic expression of SNX16 has an effect on the tumorigenic activity of this cell line. Stable MCF-7 cell lines expressing the empty vector or SNX2 are used as the control. We injected these cells into the SCID mice, monitored the sizes of the tumors and finally determined the weights of tumors 27 days post inoculation after the dissection of tumors. We found that the ectopic expression of SNX16 but not SNX2 significantly reduces the tumor formation activity of MCF-7 cells (Figure 4, P=0.001, 0.0002 and 0.27 for SNX16-1, SNX16-2 and SNX2 respectively). Together, our results suggest that SNX16 is a negative regulator of cell migration and tumorigenesis in vivo.Figure 4

Bottom Line: Ectopic expression of SNX16 reduces the migration and the tumor formation activity of MCF-7 cells.Our results indicate that, in addition to the PI3P, there is a SNX23- and microtubule-dependent cargo transport pathway required for the proper subcellular distribution of SNX16.SNX16 plays a negative regulatory role during cell migration and tumorigenesis.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Regenerative Biology, Chinese Academy of Sciences, and Guangdong Provincial Key Laboratory of Stem Cells and Regenerative Medicine, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Guangzhou, 510530 China.

ABSTRACT

Background: Sorting nexins are a large family of proteins that are associated with various components of the endosome system and they play many roles in processes such as endocytosis, intracellular protein trafficking and cell signaling. The subcellular distribution patterns of many of them remain controversial and their in vivo functions have not been characterized yet.

Results: We investigated the subcellular distribution and function of SNX16 in this study. SNX16 is detected on Rab5-positive endosomes localized adjacent to focal adhesions at cell cortex. Inhibition of SNX23, polymerization of microtubule filaments as well as the PI3-kinase all disrupt the cell cortex distribution of SNX16. Ectopic expression of SNX16 reduces the migration and the tumor formation activity of MCF-7 cells.

Conclusion: Our results indicate that, in addition to the PI3P, there is a SNX23- and microtubule-dependent cargo transport pathway required for the proper subcellular distribution of SNX16. SNX16 plays a negative regulatory role during cell migration and tumorigenesis.

No MeSH data available.


Related in: MedlinePlus