Limits...
The histone demethylase PHF8 promotes prostate cancer cell growth by activating the oncomiR miR-125b.

Ma Q, Chen Z, Jia G, Lu X, Xie X, Jin W - Onco Targets Ther (2015)

Bottom Line: Furthermore, miR-125b is a target of PHF8, and miR-125b seems to be essential for the hyper proliferation of PCa cells in the presence of PHF8.In conclusion, we identify the histone demethylase PHF8 as an oncogenic protein in human PCa.These findings indicate PHF8 as a potential candidate for clinical intervention.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, Jinshan Hospital, Fudan University, Shanghai, People's Republic of China.

ABSTRACT

Aims: Prostate cancer (PCa) is the most frequently diagnosed malignancy in men. However, the underlying mechanism is not fully understood. In this study, we aim to research the molecular mechanisms underlying the initiation and progression of PCa.

Results: Plant homeodomain finger protein 8 (PHF8) is upregulated in human PCa tissues and cell lines. PHF8 knockdown attenuates growth and cellular transformation of PCa cells. PHF8 depletion induces PCa cell apoptosis by activating proapoptotic proteins and inactivating antiapoptotic proteins. Furthermore, miR-125b is a target of PHF8, and miR-125b seems to be essential for the hyper proliferation of PCa cells in the presence of PHF8.

Conclusion: In conclusion, we identify the histone demethylase PHF8 as an oncogenic protein in human PCa. These findings indicate PHF8 as a potential candidate for clinical intervention.

No MeSH data available.


Related in: MedlinePlus

PHF8 knockdown inhibits prostate cancer cell growth in vitro and in vivo.Notes: (A–C) PHF8 knockdown attenuates human prostate cancer cell proliferation. LNCaP (A), PC-3 (B), and DU145 (C) cells were infected with retrovirus carrying sh-Ctrl or sh-PHF8, and the cell numbers were evaluated with MTT method at 24 hours, 48 hours, and 72 hours postinfection. *P<0.05, **P<0.01 vs sh-Ctrl. (D–F) Control cells or those with sh-PHF8 transduction were subjected to soft sugar colony formation assay. The number of colonies was analyzed 2 weeks later. (D) LNCaP cells, (E) PC-3 cells, and (F) DU145 cells were quantified. N=3 in each group. PHF8 knockdown represses in vivo growth of human prostate cancer cells. Control prostate cancer cells or those with sh-PHF8 transduction were subjected to xenograft mice experiments (G–I). Tumor weight was evaluated at the terminal of the experiments. (G) LNCaP cells, (H) PC-3 cells, and (I) DU145 cells were quantified. N=10 in each group.Abbreviation: PHF8, plant homeodomain finger protein 8.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4539089&req=5

f2-ott-8-1979: PHF8 knockdown inhibits prostate cancer cell growth in vitro and in vivo.Notes: (A–C) PHF8 knockdown attenuates human prostate cancer cell proliferation. LNCaP (A), PC-3 (B), and DU145 (C) cells were infected with retrovirus carrying sh-Ctrl or sh-PHF8, and the cell numbers were evaluated with MTT method at 24 hours, 48 hours, and 72 hours postinfection. *P<0.05, **P<0.01 vs sh-Ctrl. (D–F) Control cells or those with sh-PHF8 transduction were subjected to soft sugar colony formation assay. The number of colonies was analyzed 2 weeks later. (D) LNCaP cells, (E) PC-3 cells, and (F) DU145 cells were quantified. N=3 in each group. PHF8 knockdown represses in vivo growth of human prostate cancer cells. Control prostate cancer cells or those with sh-PHF8 transduction were subjected to xenograft mice experiments (G–I). Tumor weight was evaluated at the terminal of the experiments. (G) LNCaP cells, (H) PC-3 cells, and (I) DU145 cells were quantified. N=10 in each group.Abbreviation: PHF8, plant homeodomain finger protein 8.

Mentions: Since our results indicated that PHF8 is involved in human PCa, we explored whether PHF8 regulates the cellular behaviors of PCa cells. Therefore, we knocked down PHF8 in PCa cell lines, LNCaP, PC-3, and DU145. We found that PHF8 knockdown reduced cellular proliferation rate of PCa cells in vitro (Figure 2A–C). We next probed the potential contribution of PHF8 to the transformative properties of PCa cells. We observed that PHF8-depleted cells possessed reduced colony-forming activity in LNCaP, PC-3, and DU145 cells (Figure 2D–F). Furthermore, we generated prostate cells with stably PHF8 knockdown and performed xenograft experiment. The results showed that PHF8 knockdown significantly inhibited the growth of PCa cells in vivo (Figure 2G–I). These evidences demonstrate that PHF8 promotes PCa cell growth and cellular transformation.


The histone demethylase PHF8 promotes prostate cancer cell growth by activating the oncomiR miR-125b.

Ma Q, Chen Z, Jia G, Lu X, Xie X, Jin W - Onco Targets Ther (2015)

PHF8 knockdown inhibits prostate cancer cell growth in vitro and in vivo.Notes: (A–C) PHF8 knockdown attenuates human prostate cancer cell proliferation. LNCaP (A), PC-3 (B), and DU145 (C) cells were infected with retrovirus carrying sh-Ctrl or sh-PHF8, and the cell numbers were evaluated with MTT method at 24 hours, 48 hours, and 72 hours postinfection. *P<0.05, **P<0.01 vs sh-Ctrl. (D–F) Control cells or those with sh-PHF8 transduction were subjected to soft sugar colony formation assay. The number of colonies was analyzed 2 weeks later. (D) LNCaP cells, (E) PC-3 cells, and (F) DU145 cells were quantified. N=3 in each group. PHF8 knockdown represses in vivo growth of human prostate cancer cells. Control prostate cancer cells or those with sh-PHF8 transduction were subjected to xenograft mice experiments (G–I). Tumor weight was evaluated at the terminal of the experiments. (G) LNCaP cells, (H) PC-3 cells, and (I) DU145 cells were quantified. N=10 in each group.Abbreviation: PHF8, plant homeodomain finger protein 8.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4539089&req=5

f2-ott-8-1979: PHF8 knockdown inhibits prostate cancer cell growth in vitro and in vivo.Notes: (A–C) PHF8 knockdown attenuates human prostate cancer cell proliferation. LNCaP (A), PC-3 (B), and DU145 (C) cells were infected with retrovirus carrying sh-Ctrl or sh-PHF8, and the cell numbers were evaluated with MTT method at 24 hours, 48 hours, and 72 hours postinfection. *P<0.05, **P<0.01 vs sh-Ctrl. (D–F) Control cells or those with sh-PHF8 transduction were subjected to soft sugar colony formation assay. The number of colonies was analyzed 2 weeks later. (D) LNCaP cells, (E) PC-3 cells, and (F) DU145 cells were quantified. N=3 in each group. PHF8 knockdown represses in vivo growth of human prostate cancer cells. Control prostate cancer cells or those with sh-PHF8 transduction were subjected to xenograft mice experiments (G–I). Tumor weight was evaluated at the terminal of the experiments. (G) LNCaP cells, (H) PC-3 cells, and (I) DU145 cells were quantified. N=10 in each group.Abbreviation: PHF8, plant homeodomain finger protein 8.
Mentions: Since our results indicated that PHF8 is involved in human PCa, we explored whether PHF8 regulates the cellular behaviors of PCa cells. Therefore, we knocked down PHF8 in PCa cell lines, LNCaP, PC-3, and DU145. We found that PHF8 knockdown reduced cellular proliferation rate of PCa cells in vitro (Figure 2A–C). We next probed the potential contribution of PHF8 to the transformative properties of PCa cells. We observed that PHF8-depleted cells possessed reduced colony-forming activity in LNCaP, PC-3, and DU145 cells (Figure 2D–F). Furthermore, we generated prostate cells with stably PHF8 knockdown and performed xenograft experiment. The results showed that PHF8 knockdown significantly inhibited the growth of PCa cells in vivo (Figure 2G–I). These evidences demonstrate that PHF8 promotes PCa cell growth and cellular transformation.

Bottom Line: Furthermore, miR-125b is a target of PHF8, and miR-125b seems to be essential for the hyper proliferation of PCa cells in the presence of PHF8.In conclusion, we identify the histone demethylase PHF8 as an oncogenic protein in human PCa.These findings indicate PHF8 as a potential candidate for clinical intervention.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, Jinshan Hospital, Fudan University, Shanghai, People's Republic of China.

ABSTRACT

Aims: Prostate cancer (PCa) is the most frequently diagnosed malignancy in men. However, the underlying mechanism is not fully understood. In this study, we aim to research the molecular mechanisms underlying the initiation and progression of PCa.

Results: Plant homeodomain finger protein 8 (PHF8) is upregulated in human PCa tissues and cell lines. PHF8 knockdown attenuates growth and cellular transformation of PCa cells. PHF8 depletion induces PCa cell apoptosis by activating proapoptotic proteins and inactivating antiapoptotic proteins. Furthermore, miR-125b is a target of PHF8, and miR-125b seems to be essential for the hyper proliferation of PCa cells in the presence of PHF8.

Conclusion: In conclusion, we identify the histone demethylase PHF8 as an oncogenic protein in human PCa. These findings indicate PHF8 as a potential candidate for clinical intervention.

No MeSH data available.


Related in: MedlinePlus