CKS1B as a potential target for prognostic assessment and intervention in pancreatic cancer and its role in abnormal proliferation and cellular phenotype through mediation of cell cycle signaling pathways

Sep 21, 2026

Uploaded by Eliana

Study examines how the cell cycle protein-independent kinase regulatory subunit CKS1B contributes to aggressive, rapid proliferation in pancreatic cancer and its relationship with abnormal cellular phenotypes. A comprehensive bioinformatics workflow uses raw mRNA data from the Cancer Genome Atlas and Gene Expression Omnibus, assessing differential CKS1B expression in tumors and adjacent tissues. Kaplan-Meier analysis links CKS1B expression with overall survival, while RNA-interactome resources support exploration of molecular mechanisms. Elevated CKS1B is identified as a prognostic factor and connected to PKMYT1 and ATR-Chk1-Cdc25 signaling.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages11

Reading Time28 min

AccessFree to download

Abstract

Objectives

Methods

Results

Conclusion

Background and rationale

Original Article CKS1B as a potential target for prognostic assessment and intervention in pancreatic cancer and its role in abnormal proliferation and cellular phenotype through mediation of cell cycle signaling pathways Yuzhu Tang, MM, Xiaohua Lan, MM, Maohui Yan, MD, Zhiguang Fu, MD, Hongqi Li, MD, PhD. ABSTRACT الأهداف: دراسة دور الوحدة الفرعية التنظيمية للكيناز المعتمدة على بروتيندورة الخلية CKS1B في تحفيز الانتشار العدواني والسريع الذي لوحظ فيسرطان البنكرياس. المنهجية: أجري تحليل شامل باستخدام معلومات وبيانات الرنا المرسال الخاممن قاعدتي بيانات: أطلس جينوم السرطان وجامع التعبير الجيني. أجريتقييم التعبير التفاضلي لـ CKS1B في مستويات الرنا المرسال والأنسجة فيالسرطان والأنسجة المجاورة للسرطان. بالإضافة إلى ذلك، قمنا بدراسة العلاقةبين تعبير CKS1B ومعدل البقاء الإجمالي (OS) باستخدام منحنياتالبقاء لكابلان ماير. تم استكشاف الآليات الجزيئية المحتملة التي قد يؤثر بها CKS1B على الخصائص البيولوجية لسرطان البنكرياس باستخدام المواردالمتاحة في موسوعة قاعدة بيانات RNA interactomes. النتائج: أظهر CKS1B تعبيرًا تفاضليً ا كبيرًا في mRNA وكذلكمستويات البروتين. ولوحظ وجود علاقة ذات دلالة إحصائية بين تعبير CKS1B والمرحلة N والعمر واستهلاك الكحول. والجدير بالذكر أنه تم تحديدتعبير CKS1B المرتفع كعامل تنبؤي لمعدل البقاء الإجمالي. علاوة علىذلك، كشف التحليل عن دور محتمل بين CKS1B وجزيء PKMYT1،والذي يمكن أن يؤثر على مسار إشارات ATR-Chk1-Cdc25 و يعطلنقطة G2/M داخل دورة الخلية، مما يعزز في النهاية تكاثر الورم غير الطبيعي. Objectives: To investigate the role of cell cycle proteindependent kinase regulatory subunit 1B )CKS1B( in driving the aggressive and rapid proliferation observed in pancreatic cancer. Methods: A comprehensive analysis was carried out using raw mRNA information and data from 2 databases: the cancer genome atlas and gene expression omnibus. The differential expression of CKS1B at the mRNA and tissue levels in cancer and adjacent paracancerous tissues were assessed. Additionally, the relationship of CKS1B expression and overall survival )OS( rate was investigated using Kaplan-Meier survival curves. Potential molecular mechanisms by which CKS1B may influence the biological characteristics of pancreatic cancer were explored using resources available within the encyclopedia of RNA interactomes database. Results: The CKS1B exhibited significant differential expression at the mRNA as well as protein levels. A correlation with statistical significance between CKS1B expression and N stage, age, and alcohol consumption was observed. Notably, high CKS1B expression was determined as a predictive factor for worse OS. Furthermore, the analysis revealed a potential synergistic role between CKS1B and the molecule PKMYT1, which could impact the ATRChk1-Cdc25 signaling pathway and disrupt the G2/M checkpoint within the cell cycle, ultimately promoting abnormal tumor proliferation. Conclusion: The CKS1B may serve as a novel potential prognostic factor in pancreatic cancer and is involved in the abnormal proliferation biology phenotype by mediating cell cycle signaling pathways. Keywords: pancreatic cancer, regulatory subunit 1B, PKMYT1, microRNAs Saudi MedJ 2024; Vol. 45 (2): 128-138 doi: 10.15537/smj.2024.45.2.20230132 From the Department of specialty (Yuzhu, Xiaohua), Graduate School of Hebei North University, Zhangjiakou, andfrom the Department of Radiation Oncology (Yuzhu, Maohui, Zhiguang, Hongqi), Air Force Medical Center, PLA, Beijing, China. Received 26th April 2023. Accepted 4th January 2024. Address correspondence and reprint request to: Dr. Li Hongqi, Departmrnt of Radiation Oncology, Air Force Medical Center, PLA, Beijing, China. E-mail: [lihongqi2023@sina.com](lihongqi2023@sina.com) ORCID ID: [https://orcid.org/0000-0001-6944-701X](https://orcid.org/0000-0001-6944-701X) Pnhcerefiatelicd coafnceroncopologsey,s a formidable challenge in presenting a serious threat to human life and well-being. The latest American cancer statistics for 2022 reveal that pancreatic cancer stands as the fifth leading cau

FAQs

What is the main research goal regarding CKS1B in pancreatic cancer?

To investigate how CKS1B may drive aggressive, rapid proliferation and contribute to abnormal cellular phenotypes in pancreatic cancer.

How was CKS1B expression and its prognostic value assessed?

The study used bioinformatics analyses on raw mRNA and tissue data from TCGA and GEO, and evaluated associations with overall survival using Kaplan-Meier survival curves.

What molecular pathway connection did the analysis suggest for CKS1B?

High CKS1B expression was linked to worse overall survival and to a potential synergistic role with PKMYT1, impacting the ATR-Chk1-Cdc25 signaling pathway and disrupting the G2/M checkpoint.

Sep 21, 2026

Uploaded by Eliana