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第 57 卷第 1 期 葛 姮,等:五氟利多靶向 HSPA6 抑制黑色素瘤生长的作用研究 77
A B C **
Model si-NC+Penfluridol Model 125
800 Penfluridol si-HSPA6 100
si-NC si-HSPA6+Penfluridol Penfluridol 75
Tumor Size Variations compared to 0 day/% 400 si-NC+Penfluridol Mean tumor volume compared to control group/% 50 0
600
si-NC
25
si-HSPA6
si-HSPA6+Penfluridol
si-NC
200
0 si-HSPA6+Penfluridol Model Penfluridol si-NC+Penfluridol si-HSPA6
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14
t/d
Figure 7 Tumor growth inhibition induced by penfluridol depends on the presence of HSPA6 ( x ± s,n=5)
A: Tumor growth kinetics [Tumor volumes are shown relative to the tumor volume in mice before treatment (set as "1")]; B: Representative
photographs of excised tumors; C: Terminal tumor volume comparison [Tumor volumes are shown as a percentage relative to the Model group
(set as 100%)]
**P < 0.01
当 HSPA6 表达被抑制时,其对 p53 的影响作用减 sion in breast cancer through induction of reactive oxygen
species and downregulation of sp transcription factors[J]. Mol
弱,进而削弱五氟利多对促凋亡通路的激活效应。 Cancer Ther, 2017, 16(1): 205-216.
综上,五氟利多可显著抑制黑色素瘤细胞的增 [10] Shaw V, Srivastava S, Srivastava SK. Repurposing antipsy-
殖,导致细胞发生 G 期阻滞,诱导细胞发生凋亡, chotics of the diphenylbutylpiperidine class for cancer
1
therapy[J]. Semin Cancer Biol, 2021, 68: 75-83.
其分子机制可能与上调细胞内 HSPA6、p53、p21 的 [11] Lai TC, Lee YL, Lee WJ, et al. Synergistic tumor inhibition via
表达有关。本研究不仅扩大了五氟利多的治疗广 energy elimination by repurposing penfluridol and 2-deoxy-D-
glucose in lung cancer[J]. Cancers (Basel), 2022, 14(11): 2750.
度,还为黑色素瘤的治疗提供新的治疗手段。
[12] Cheikh IA, Hayar B, Ghanem N, et al. Therapeutic targeting of
the pentose phosphate pathway in colorectal cancer using 6-
aminonicotinamide and 5-fluorouracil[J]. Mol Carcinog, 2025,
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