Research ArticleExperimental Studies
Open Access

Impact of Cyclin-dependent Kinase Inhibitor 1A Genotypes on Prostate Cancer Susceptibility Prediction

CHENG-HSI LIAO, DA-TIAN BAU, BO-REN WANG, SHU-YU CHANG, TE-CHUN HSIA, HSU-TUNG LEE, JAW-CHYUN CHEN, WEN-CHIN HUANG, CHIA-WEN TSAI, YUN-CHI WANG, HOU-YU SHIH and WEN-SHIN CHANG
In Vivo November 2025, 39 (6) 3184-3194; DOI: https://doi.org/10.21873/invivo.14118

Abstract

Background/Aim: Prostate cancer is a multifactorial disease influenced by both genetic and environmental factors. Previous studies have identified a correlation between p21 expression and the clinical severity of prostate cancer. However, the contribution of cyclin-dependent kinase inhibitor 1A (CDKN1A), which encodes p21, to prostate cancer susceptibility remains unclear. This study aimed to evaluate the association between CDKN1A polymorphisms rs1801270 and rs1059234 and the risk of prostate cancer in a Taiwanese population.

Patients and Methods: A total of 218 patients with prostate cancer and 436 cancer-free controls were genotyped for CDKN1A rs1801270 and rs1059234 using the PCR-RFLP method. Genotypic distributions were analyzed for associations with prostate cancer risk overall and stratified by age and smoking status.

Results: No significant association was observed between either CDKN1A rs1801270 or rs1059234 genotypes and overall prostate cancer risk (both p>0.05). However, stratified analysis showed that individuals aged <55 years carrying the rs1801270 variant genotypes (AC and AA) had a significantly increased risk of early-onset prostate cancer [odds ratio (OR)=2.16 and 2.51, 95% confidence interval (CI)=1.25-3.71 and 1.37-4.61, p=0.0069 and 0.0041, respectively]. Additionally, among non-smokers, carriers of the rs1059234 variant genotypes (CT and TT) exhibited a significantly reduced prostate cancer risk (OR=0.27 and 0.36, 95%CI=0.11-0.64 and 0.14-0.98, p=0.0042 and 0.0739, respectively), indicating a potential gene-environment interaction.

Conclusion: While CDKN1A rs1801270 and rs1059234 may not serve as general predictive markers for prostate cancer susceptibility, they appear to modulate prostate cancer risk under specific age and smoking contexts. These findings merit further validation in larger and ethnically diverse populations and may contribute to more refined risk stratification and personalized prevention strategies.

Keywords:

Introduction

Prostate cancer ranks as the second most frequently diagnosed malignancy in men globally and remains a major contributor to cancer-associated deaths (1, 2). Its incidence continues to rise, particularly in industrialized nations. In the United States alone, projections for 2025 estimate approximately 313,780 new diagnoses and 35,770 fatalities (3). Early detection of prostate cancer remains a clinical challenge, and its etiology is believed to be multifactorial. Epidemiological evidence implicates a range of potential risk factors, including familial predisposition, ethnic background, occupational exposures, cadmium contact, vasectomy history, obesity, and alcohol intake. Among these, genetic determinants are thought to exert a substantial, though not yet fully elucidated, influence (4-8). Our prior research has contributed to this field by conducting a genome-wide screening of prostate cancer susceptibility loci (9), as well as identifying several candidate genes relevant to Taiwanese population (10-15). Despite these advances, our understanding of the genetic underpinnings associated with disease progression and prognosis remains inadequate, underscoring the need for continued and more comprehensive genomic investigations.

The p21 protein, encoded by the cyclin-dependent kinase inhibitor 1A (CDKN1A) gene situated at chromosome 6p21, is a well-characterized cyclin-dependent kinase inhibitor also known by various aliases including WAF1, CAP20, Cip1, and Sdi1 (16). Two widely investigated single nucleotide polymorphisms (SNPs) in CDKN1A have garnered attention due to their potential functional significance. The first involves a non-synonymous substitution at codon 31, where a serine (C allele) is replaced by arginine (A allele, rs1801270), and the second is a C-to-T base transition located 20 base pairs downstream of the stop codon (rs1059234) (17, 18). Notably, rs1801270 consolidates previous SNP identifiers rs17851079, rs17849556, and rs3176351, whereas rs1059234 integrates rs56592857, rs3800367, and rs3167770. These variants have been proposed to influence the biological function of p21 (19). Extensive research has explored associations between CDKN1A polymorphisms and the risk of various malignancies, encompassing breast (20), lung (21, 22), head and neck (18), oral (23), esophageal (24-26), gastric (27-29), liver (30), pancreatic (31), ovarian (32, 33), cervical (34) endometrial (35-37), and bladder cancer (38). Some of these studies reported statistically significant associations between the aforementioned SNPs and increased cancer susceptibility, while others failed to confirm any meaningful relationship in cancers such as breast (39), oral (40), nasopharyngeal (41), esophageal (25, 42), thyroid (43), colorectal (44-47), cervical (48), ovarian (33), bladder cancer (49), retinoblastoma (50), and leukemia (51). Taken together, these findings suggest that rs1801270 and rs1059234 variants in CDKN1A may contribute to cancer susceptibility, though their role appears to be context- and tissue-specific. Given the biological relevance of p21 in cell cycle control and DNA damage response, it is plausible that these polymorphisms could also influence the risk of prostate cancer. However, despite the extensive research conducted on other malignancies, investigations focusing specifically on the association between CDKN1A genotypes and prostate cancer remain limited, warranting further in-depth exploration.

Therefore, to elucidate the potential contribution of CDKN1A polymorphisms to prostate cancer susceptibility in the Taiwanese population, we conducted a genotypic analysis of two common variants, rs1801270 and rs1059234 (Figure 1), in a representative cohort of patients with prostate cancer. Furthermore, we sought to explore the potential interactive effects between these CDKN1A genotypes and key epidemiological factors, particularly age and smoking status, in relation to prostate cancer risk.

Figure 1.
Figure 1.

Physical map for CDKN1A rs1801270 and rs1059234 polymorphic sites.

Patients and Methods

Recruited prostate cancer-specific Taiwan cohort. A total of 218 male patients diagnosed with prostate cancer were recruited from China Medical University Hospital, a major medical center located in central Taiwan. For comparison, a control group comprising twice the number of cancer-free individuals (n=436) was selected from the hospital’s Health Examination Cohort. All participants were of Taiwanese ethnicity, provided written informed consent, and donated 3-5 ml of peripheral blood for genomic DNA extraction and genotyping. The inclusion and exclusion criteria for both groups have been described in detail in prior publications (9, 10). The study protocol was reviewed and approved by the Institutional Review Board of China Medical University Hospital (CMUH110-REC3-005). Demographic and clinical characteristics of the study population are summarized in Table I, including age distribution, smoking behavior, family history of cancer, disease stage, and histological grade. As expected, there was no significant difference in age distribution between prostate cancer cases and controls (<55 versus ≥55 years), reflecting the matched design of the study (p=0.67). Similarly, smoking habits did not significantly differ between the two groups (p=0.27). Regarding familial cancer history, 7.8% and 1.8% of patients with prostate cancer reported having first- and second-degree relatives, respectively, with a history of malignancy. Among the patients with prostate cancer, 71.1% were diagnosed at early stages, while 28.9% presented with advanced disease. In terms of pathological grading, 12.9% of tumors were well-differentiated, 40.8% were moderately differentiated, and 46.3% were poorly differentiated (Table I).

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Table I.

Demographics of the prostate cancer cases and the control subjects.

CDKN1A genotyping methodology and imputation. Genomic DNA was isolated from the peripheral blood samples of all participants using a standardized protocol established in our previous studies (52, 53). Genotyping of the CDKN1A polymorphisms rs1801270 and rs1059234 was carried out following established procedures as described in our earlier publications (51, 54). Details regarding the primer sequences, polymerase chain reaction (PCR) conditions, and restriction fragment length polymorphism (RFLP) analysis are provided in Table II. The chromosomal positions of the two SNPs within the CDKN1A gene are illustrated in Figure 1. In brief, PCR amplification for both SNPs was conducted using the following cycling parameters, an initial denaturation at 95°C for 5 min; 35 cycles of denaturation at 95°C for 30 s, annealing at 55°C for 30 s, and extension at 72°C for 30 s; followed by a final elongation at 72°C for 10 min. For rs1801270, the primer pair used was 5′-GTCAGAACCGGCTGGGGATG-3′ (forward) and 5′-CTCCTCCCAACTCATCCCGG-3′ (reverse). For rs1059234, the primer sequences were 5′-TCCAAGAGG AAGCCCTAATC-3′ (forward) and 5′-AAAGGAGAACACGGG ATGAG-3′ (reverse). The PCR products were subjected to enzymatic digestion using Blp I for rs1801270 and Pst I for rs1059234 (New England BioLabs, Ipswich, MA, USA), with incubation at 37°C for 16 h. Digestion products were resolved on 3% agarose gels and visualized under UV light. The genotypes of CDKN1A rs1801270 were distinguished as CC (63 bp+186 bp), AC (63 bp+186 bp+249 bp), and AA (249 bp). For CDKN1A rs1059234, the CC, CT, and TT genotypes produced bands of 39 bp+257 bp, 39 bp+257 bp+296 bp, and 296 bp, respectively.

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Table II.

The primer sequences, polymerase chain reaction and restriction fragment length polymorphism methodology for identifying CDKN1A rs1801270 and rs1059234 genotypes.

Statistical analysis. Statistical analyses were performed using the Student’s t-test to evaluate differences in mean age between prostate cancer cases and non-cancerous controls. The associations between CDKN1A rs1801270 and rs1059234 genotypes and prostate cancer risk were assessed using Pearson’s Chi-square test. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated to estimate the strength of the associations. All statistical tests were two-tailed, and a p-value of less than 0.05 was considered indicative of statistical significance.

Results

Contributions of CDKN1A polymorphic genotypes to prostate risk. In this case-control study, the distribution of CDKN1A rs1801270 and rs1059234 genotypes was analyzed in 218 prostate cancer cases and 436 cancer-free controls from a Taiwanese population. As shown in Table III, genotype frequencies in the control group for both rs1801270 and rs1059234 conformed to Hardy-Weinberg equilibrium (HWE) (p=0.8352 and 0.4650, respectively), indicating appropriate population representation. Analysis of rs1801270 revealed no significant difference in genotype distribution between patients with prostate cancer and controls (ptrend=0.2214; Table III upper part). Specifically, carriers of the AA homozygous variant and the AC heterozygous genotype did not exhibit significantly increased prostate cancer risk compared to the CC reference group (the results for AA and AC are OR=1.49 and 1.32, 95%CI=0.93-2.37 and 0.88-1.97, p=0.1194 and 0.2118, respectively; Table III upper part). Similarly, the dominant model (AA+AC vs. CC) showed no significant association with disease susceptibility (OR=1.37, 95%CI=0.94-2.00, p=0.1246; Table III upper part). Likewise, no significant association was observed between rs1059234 genotypes and prostate cancer risk (ptrend=0.6553; Table III lower part). Compared to the CC genotype, individuals carrying the TT homozygous or CT heterozygous variants showed a statistically significant change in risk (the results for TT and CT are OR=0.80 and 0.89, 95%CI=0.50-1.29 and 0.61-1.30, p-value=0.4341 and 0.6049, respectively; Table III lower part). The dominant genetic model (TT+CT versus CC) also yielded non-significant results (OR=0.86, 95%CI=0.60-1.24, p=0.4780).

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Table III.

Distributions of CDKN1A rs1801270 and rs1059234 genotypic frequencies among patients with prostate cancer and healthy controls.

Contributions of CDKN1A allelic patterns to prostate cancer risk. The allelic frequencies of the CDKN1A rs1801270 and rs1059234 polymorphisms were further analyzed among the prostate cancer cases and non-cancerous controls (Table IV). Consistent with the genotypic findings presented in Table III, no significant differences in allelic distributions were observed between the prostate cancer and control groups. Specifically, the A allele of rs1801270 and the T allele of rs1059234 were not associated with altered prostate cancer risk (OR=1.15 and 0.90, 95%CI=0.92-1.45, and 0.71-1.13, p=0.2483 and 0.3993, respectively; Table IV). These results further suggest that neither CDKN1A rs1801270 nor rs1059234 alleles can serve as predictive biomarkers for prostate cancer susceptibility in the Taiwanese population.

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Table IV.

Allelic frequencies for CDKN1A rs1801270 and rs1059234 polymorphisms in patients with prostate cancer and control groups.

Association of CDKN1A genotypes with Taiwan prostate risk stratified by age and smoking status. We further evaluated the association between CDKN1A rs1801270 and rs1059234 genotypes and prostate cancer risk by stratifying the data according to age and smoking status (Table V and Table VI). Notably, individuals younger than 55 years carrying the AC and AA genotypes of CDKN1A rs1801270 exhibited a significantly increased risk of developing prostate cancer compared to those with the CC genotype (OR=2.16 and 2.51, 95%CI=1.25-3.71 and 1.37-4.61, p=0.0069 and 0.0041, respectively). In contrast, no significant associations were observed between CDKN1A rs1801270 genotypes and prostate cancer risk among individuals aged 55 years or older (both p>0.05; Table V). Additionally, no significant differences in rs1801270 genotype distribution were found between smokers and non-smokers, regardless of heterozygous or homozygous variant status (Table V). As for CDKN1A rs1059234, the CT and TT genotypes were significantly more frequent in the prostate cancer group than in controls (OR=1.95 and 2.43, 95%CI=1.15-3.31 and 1.33-4.44, p=0.0170 and 0.0056, respectively). Interestingly, among non-smokers, the same CT and TT genotypes appeared to be associated with a reduced risk of prostate cancer, suggesting a potential protective effect (OR=0.27 and 0.36, 95%CI=0.11-0.64 and 0.14-0.98, p=0.0042 and 0.0739, respectively).

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Table V.

Association of CDKN1A rs1801270 genotypes with prostate cancer risk stratified by age and smoking status compared with non-cancerous healthy controls.

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Table VI.

Association of CDKN1A rs1059234 genotypes with prostate cancer risk stratified by age and smoking status compared with non-cancerous healthy controls.

Discussion

In literature, several studies have investigated the association between CDKN1A genotypes and prostate cancer susceptibility. In 2003, Kibel and his colleagues reported that the CDKN1A rs1059234 CT and TT genotypes were associated with an increased risk of advanced prostate carcinoma in a mixed European-American population, particularly in cases of aggressive metastatic disease (55). In 2004, Huang and his co-workers provided supporting evidence with similar findings (56). In 2013, Sivoňová and his colleagues have shifted the focus to the CDKN1A rs1059234 polymorphism (57), located within the 3′ untranslated region (3′ UTR), 20 nucleotides downstream of the stop codon. This variant has been hypothesized to influence cancer risk by altering mRNA stability and thus affecting intracellular levels of the p21 protein (18). However, their findings did not support an association between CDKN1A rs1059234 genotypes and prostate cancer risk in a pilot study (57), and this result was further validated by the same research group in a follow-up study two years later (58).

In this study, we examined the association between two commonly studied CDKN1A polymorphisms, rs1801270 and rs1059234, and prostate cancer risk in a Taiwanese cohort comprising 218 patients with prostate cancer and 436 healthy controls. Genotyping results revealed no significant association between the variant genotypes of either rs1801270 or rs1059234 and prostate cancer susceptibility (Table III and Table IV). These findings differ from earlier studies that reported a positive association between CDKN1A rs1801270 genotypes and prostate cancer risk, notably those by Kibel’s and Huang’s teams (55, 56). First, the discrepancy with the findings of Kibel’s group may largely stem from differences in the studied ethnic populations. Additionally, their sample size was smaller than ours (controls:cases=106:96 versus 436:218), and the distribution of CDKN1A rs1801270 genotypes among their controls deviated from HWE (pHWE=0.007), which may limit the reliability of their results. Second, while Huang’s study and ours both targeted Taiwanese populations with comparable sample sizes (controls:cases=247:200 vs. 436:218), they reported a borderline significant association between the rs1801270 AA genotype and increased prostate cancer risk (OR=1.77, 95%CI=1.06-2.94, p=0.0377). Our findings showed a similar trend, though not statistically significant (OR=1.49, 95%CI=0.93-2.37, p=0.1194). Notably, the hospital in Huang’s study is located in southern Taiwan, an area with a potentially higher proportion of aboriginal individuals, whereas our cohort was recruited from central Taiwan. When the data from both studies are combined, a significant association emerges (OR=1.59, 95%CI=1.14-2.24, p=0.0088), which may better reflect the genetic profile of the overall Taiwanese population. Lastly, Sivoňová and his colleagues reported no association between CDKN1A rs1801270 and prostate cancer risk in their Slovak population (58) further suggesting potential ethnic differences in genetic susceptibility. Collectively, these findings indicate that the role of CDKN1A rs1801270 in prostate cancer warrants further investigation, particularly in larger, ethnically diverse populations. As for rs1059234, consistent with previous reports (57, 58), no significant association with prostate cancer risk was identified in our study.

Established risk factors for prostate cancer include ethnicity, age, family history, genetic predisposition, diet, and smoking behavior (59-63). First, significant disparities exist in prostate cancer incidence among ethnic groups; for example, African-American men exhibit substantially higher prevalence and mortality rates compared to most other populations (64, 65). Second, given that age is a critical determinant of prostate cancer risk, we performed stratified analyses to assess potential synergistic effects between CDKN1A genotypes and age. Our results demonstrated that the impact of both rs1801270 and rs1059234 genotypes on prostate cancer susceptibility was more pronounced among individuals younger than 55 years (Table V and Table VI). This observation partially aligns with findings from Huang and Kibel, who reported a stronger association between the rs1801270 AA genotype and prostate cancer risk in younger men (55, 56). Third, smoking is recognized as an environmental risk factor contributing to increased prostate cancer incidence (66, 67). Our stratified analyses revealed that the variant CT and TT genotypes of CDKN1A rs1059234 may confer a protective effect among non-smokers, an effect that was not observed in smokers (Table VI). In contrast, rs1801270 genotypes showed no significant influence on prostate cancer risk irrespective of smoking status (Table V). Previous work by Sivoňová et al. reported that smokers carrying the CT and TT genotypes at rs1059234 had increased prostate cancer risk, whereas non-smokers with the CT genotype exhibited reduced risk (57). Collectively, these findings tentatively suggest a protective role of CDKN1A rs1059234 variants that merits further validation. Regarding rs1801270, the AC genotype was reported to have a statistically significant protective effect against prostate cancer among non-smokers (58).

In conclusion, our analysis showed that neither the genotypic nor allelic frequencies of CDKN1A rs1801270 and rs1059234 differed significantly between patients with prostate cancer and healthy controls, indicating no overall association with prostate cancer susceptibility in this population. This comprehensive study consolidates current understanding of CDKN1A rs1801270 and rs1059234 in prostate cancer, emphasizing the potential role of CDKN1A rs1801270 and rs1059234 genotypes in the synergistic interactions with younger ages and smoking behaviors. Collectively, these results highlight the nuanced role of CDKN1A polymorphisms in prostate cancer etiology, emphasizing the need for larger, multiethnic studies to clarify their clinical relevance. Additionally, our findings suggest that age and smoking status may modulate the impact of CDKN1A genetic variants, which could inform risk stratification and personalized prevention strategies in Taiwanese and other populations.

Acknowledgements

The Authors are grateful to the colleagues at Tissue Bank of China Medical University Hospital for their excellent sample and data collection. The technical assistance from Ai-Chia Tung is appreciated. This study was supported by research grant from Taichung Armed Forces General Hospital (TCAFGH-D-114010).

Footnotes

  • Authors’ Contributions

    Research design: Bau DT, Liao CH and Tsai CW; patient and questionnaire summaries: Liao CH, Wang BR and Chang SY; experimental work: Chang SY, Wang YC and Shih HY; statistical analysis: Hsia TC, Lee HT, and Tsai CW; data clearance and validation: Wang YC, Chen JC, Tsai CW and Huang WC; article writing: Liao CH, Tsai CW, Bau DT and Chang WS; correction of manuscript: Wang BR and Chang WS; review and revision: Tsai CW, Chang WS and Bau DT.

  • Conflicts of Interest

    The Authors declare no conflicts of interest in regard to the current study.

  • Artificial Intelligence (AI) Disclosure

    No artificial intelligence tools, including large language models or machine learning software, were used in the preparation, analysis, or presentation of this manuscript.

  • Received August 5, 2025.
  • Revision received August 25, 2025.
  • Accepted August 26, 2025.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY-NC-ND) 4.0 international license (https://creativecommons.org/licenses/by-nc-nd/4.0).

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Impact of Cyclin-dependent Kinase Inhibitor 1A Genotypes on Prostate Cancer Susceptibility Prediction
CHENG-HSI LIAO, DA-TIAN BAU, BO-REN WANG, SHU-YU CHANG, TE-CHUN HSIA, HSU-TUNG LEE, JAW-CHYUN CHEN, WEN-CHIN HUANG, CHIA-WEN TSAI, YUN-CHI WANG, HOU-YU SHIH, WEN-SHIN CHANG
In Vivo Nov 2025, 39 (6) 3184-3194; DOI: 10.21873/invivo.14118
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