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. 2023 Mar 16;14(2):149-152.
doi: 10.1093/procel/pwac003.

RNA helicase MTR4 drives tumorigenesis of nasopharyngeal carcinoma by regulating the expression of key cell cycle genes

Lili Yu  1   2   3 , Lei Jiang  4 , Meng Wu  1 , Wenlong Dou  4 , Kaiyuan Ji  4 , Jianlong Zhou  4 , Jinchul Kim  5 , Yang Xu  1
Affiliations

RNA helicase MTR4 drives tumorigenesis of nasopharyngeal carcinoma by regulating the expression of key cell cycle genes

Lili Yu et al. Protein Cell. .
No abstract available

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Figures

Figure 1.
Figure 1.
MTR4 is overexpressed in NPCs and required for NPC tumorigenesis. (A) Chips of NPC samples were stained with anti-MTR4 antibody and the intensity of the staining scanned and scored. Representative immunohistochemistry (IHC) images are shown. (B) The MTR4 expression levels were inversely correlated with the postoperative recurrence-free survival (RFS) of NPC patients. The differences in survival rates were assessed with the log-rank test (Mantel Cox). The survival probability of the patients with high MTR4 mRNA levels is significantly lower than those with lower MTR4. n = 20 for MTR4high tumors. n = 103 for MTR4low tumors. P value is indicated. (C) Box plot showing the relative mRNA levels of MTR4 in NPC tissues and non-tumor tissues from GSE13597 dataset. The significance was assessed by two-tailed, unpaired t-test and P value is indicated. Centre is median, bounds of the box spans the interquartile range (from 25% to 75% percentile), and whiskers visualize minima and maxima. (D) The volumes and (E) the weight of the tumors formed by NPC cells expressing non-specific scramble shRNA (SC) or MTR4 specific shRNA cells in NSG mice were measured for each group. n = 6. Values represent the mean ± s.d. Repeated measures two-way ANOVA, followed by Bonferroni post-tests. ***P < 0.001. (F) The volumes and (G) the weight of tumors formed by control NPC cells or MTR4 overexpressed (OE) cells in NSG mice were measured for each group. n = 7. Values represent the mean ± s.d. Repeated measures two-way ANOVA, followed by Bonferroni post-tests. At the end of the treatment, the weight of all tumors in each group was compared. n = 7 for each group. Values represent the mean ± s.d. Mann-Whitney test. *P < 0.05. (H) The volumes and (I) the weight of tumors formed by MTR4+/+ or MTR4+/− cells in nude mice were measured for each group. n = 10. Only 2 of 10 implanted MTR4+/− NPC cells developed detectable tumors. Values represent the mean ± s.d. Repeated measures two-way ANOVA, followed by Bonferroni post-tests. At the end of the treatment, the weight of all tumors in each group was compared. n = 10. Values represent the mean ± s.d. Mann-Whitney test. ***P < 0.001. (J) The volumes and (K) the weight of NPC PDX tumors after MTR4 KD and scramble control. n = 4. Values represent the mean ± s.d. Repeated measures two-way ANOVA, followed by Bonferroni post-tests. *P < 0.05.
Figure 2.
Figure 2.
MTR4 promotes cellular proliferation of NPCs. (A) Heat map of the mRNA expression profile in cell cycle pathway genes in MTR4 inducible knockdown (iMTR4) cells before and after Doxy treatment. (B–G) The expression levels of MTR4 in NPC tissues were correlated to the expression levels of genes with key roles in cell cycle from the GSE13597 dataset. (H) pre-mRNAs bound by MTR4 were identified by RIP-seq analysis. (I) RIP analysis to confirm the binding of MTR4 to the CDK2 pre-mRNA. A schematic of CDK2 gene displaying a potential binding motif of MTR4 indicated by an asterisk. n = 2. (J) The levels of pre-mRNA and mRNA of CDK2 in MTR4 KD cells versus control cells were detected by semi-quantitative PCR and normalized by actin levels. n = 3. Values represent means ± s.d. *P < 0.05 and **P < 0.01. (K, L) The volumes (K) and the weight (L) of tumors formed by indicated cells in NSG mice were measured (n = 8 or n = 10 for each group). Two-way ANOVA, followed by Bonferroni post-tests. *P < 0.05 and **P < 0.01.
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