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. 2022 Apr 29;14(9):2239.
doi: 10.3390/cancers14092239.

Template-Independent Poly(A)-Tail Decay and RNASEL as Potential Cellular Biomarkers for Prostate Cancer Development

Gordana Kocić  1 , Jovan Hadzi-Djokić  2 , Andrej Veljković  1 , Stefanos Roumeliotis  3 , Ljubinka Janković-Veličković  4 , Andrija Šmelcerović  5
Affiliations

Template-Independent Poly(A)-Tail Decay and RNASEL as Potential Cellular Biomarkers for Prostate Cancer Development

Gordana Kocić et al. Cancers (Basel). .

Abstract

The post-transcriptional messenger RNA (mRNA) decay and turnover rate of the template-independent poly(A) tail, localized at the 3'-untranslated region (3'UTR) of mRNA, have been documented among subtle mechanisms of uncontrolled cancer tissue growth. The activity of Poly(A) deadenylase and the expression pattern of RNASEL have been examined. A total of 138 prostate tissue specimens from 46 PC patients (cancer specimens, corresponding adjacent surgically healthy tissues, and in their normal counterparts, at least 2 cm from carcinoma) were used. For the stratification prediction of healthy tissue transition into malignant phenotype, the enzyme activity of tumor-adjacent tissue was considered in relation to the presence of microfocal carcinoma. More than a four-times increase in specific enzyme activity (U/L g.prot) was registered in PC on account of both the dissociation of its inhibitor and genome reprogramming. The obtained ROC curve and Youden index showed that Poly(A) deadenylase identified PC with a sensitivity of 93.5% and a specificity of 94.6%. The RNASEL expression profile was raised significantly in PC, but the sensitivity was 40.5% and specificity was 86.9%. A significantly negative correlation between PC and control tissue counterparts with a higher expression pattern in lymphocyte-infiltrated samples were reported. In conclusion, significantly upregulated Poly(A) deadenylase activity may be a checkpoint for the transition of precancerous lesion to malignancy, while RNASEL may predict chronic inflammation.

Keywords: RNASEL; poly(A) deadenylase; prostate cancer.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Poly(A) deadenylase specific enzyme activity (U/L g.prot) in PC, tumor adjacent with MC, tumor-adjacent and control healthy counterparts.
Figure 2
Figure 2
Receiver operating characteristic curve showing the performance of Poly(A) deadenylase specific activity in predicting prostate cancer.
Figure 3
Figure 3
Total, free, and inhibitor-bound (latent) Poly(A) deadenylaseactivity(U/L) in PC, tumor adjacent with MC, tumor-adjacent, and control healthy counterparts.
Figure 4
Figure 4
RNASEL total (ng/L) and specific (ng/g.prot) expression level in PC, tumor-adjacent, and control healthy counterparts.
Figure 5
Figure 5
Receiver operating characteristic curve showing the performance of RNASEL-specific expression in predicting prostate cancer.
Figure 6
Figure 6
RNASEL correlation between values in PC and corresponding control specimens of healthy tissue.
Figure 7
Figure 7
RNASEL in PC, tumor-adjacent and corresponding healthy tissues in relation to the presence and the type of inflammation.
Figure 8
Figure 8
Histological findings of PC, tumor-adjacent tissue with microfocal carcinoma, tumor-adjacent, and control healthy tissue specimens.
See this image and copyright information in PMC

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