Upregulation of PKN1 as a Prognosis Biomarker for Endometrial Cancer

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Abstract

Background

Several markers of survival among endometrial cancer (EC) patients have been proposed, namely, the oncoprotein stathmin, RAF kinase inhibitor (RKIP), Cyclin A, GATA-binding protein 3 (GATA3), and growth and differentiation factor-15 (GDF-15). Their elevated expression correlated significantly with a high stage, serous papillary/clear cell subtypes, and aneuploidy. In a previous study, we reported the elevated expression of the serine/threonine protein kinase N1 (PKN1) in cancerous cells. In the present paper, we studied PKN1 expression in EC tissues from a large cohort of patients, to determine whether PKN1 can serve as a marker for the aggressiveness and prognosis of EC, and/or as a marker of survival among EC patients.

Methods

Tissue samples from EC patients were examined retrospectively for tumor type, tumor size, FIGO stage and grade, depth of invasion in the myometrium, and presence of lymph node metastasis. The PKN1 protein expression in EC cells was assessed by immunohistochemistry. PKN1 mRNA levels were analyzed in publicly available databases, using bioinformatic tools.

Results

We found that expression of PKN1 at the mRNA and proteins levels tended to increase in high-grade EC samples (P = .0001 and P = .06, respectively). In addition, patients with metastatic disease had higher PKN1 mRNA levels (P = .02). Moreover, patients with high PKN1 expression could be characterized by poorer survival.

Conclusions

We have shown a trend of the higher PKN1 expression levels in EC patients with poor prognosis. Therefore, PKN1 might be considered as a candidate prognostic marker for EC.

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Most cited references 23

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Cancer statistics, 2019

Rebecca Siegel, Kimberly D Miller, Ahmedin Jemal (2019)

Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States and compiles the most recent data on cancer incidence, mortality, and survival. Incidence data, available through 2015, were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data, available through 2016, were collected by the National Center for Health Statistics. In 2019, 1,762,450 new cancer cases and 606,880 cancer deaths are projected to occur in the United States. Over the past decade of data, the cancer incidence rate (2006-2015) was stable in women and declined by approximately 2% per year in men, whereas the cancer death rate (2007-2016) declined annually by 1.4% and 1.8%, respectively. The overall cancer death rate dropped continuously from 1991 to 2016 by a total of 27%, translating into approximately 2,629,200 fewer cancer deaths than would have been expected if death rates had remained at their peak. Although the racial gap in cancer mortality is slowly narrowing, socioeconomic inequalities are widening, with the most notable gaps for the most preventable cancers. For example, compared with the most affluent counties, mortality rates in the poorest counties were 2-fold higher for cervical cancer and 40% higher for male lung and liver cancers during 2012-2016. Some states are home to both the wealthiest and the poorest counties, suggesting the opportunity for more equitable dissemination of effective cancer prevention, early detection, and treatment strategies. A broader application of existing cancer control knowledge with an emphasis on disadvantaged groups would undoubtedly accelerate progress against cancer.

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A pathology atlas of the human cancer transcriptome

Jochen Schwenk, Mathias Uhlén, Cheng Cheng Zhang … (2018)

Cancer is one of the leading causes of death, and there is great interest in understanding the underlying molecular mechanisms involved in the pathogenesis and progression of individual tumors. We used systems-level approaches to analyze the genome-wide transcriptome of the protein-coding genes of 17 major cancer types with respect to clinical outcome. A general pattern emerged: Shorter patient survival was associated with up-regulation of genes involved in cell growth and with down-regulation of genes involved in cellular differentiation. Using genome-scale metabolic models, we show that cancer patients have widespread metabolic heterogeneity, highlighting the need for precise and personalized medicine for cancer treatment. All data are presented in an interactive open-access database (www.proteinatlas.org/pathology) to allow genome-wide exploration of the impact of individual proteins on clinical outcomes.

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Two pathogenetic types of endometrial carcinoma.

J Bokhman (1983)

The author presents a hypothesis that the complex of endocrine and metabolic disturbances arising long before the development of endometrial carcinoma determines the biological peculiarities of the tumor, its clinical course, and the prognosis of the disease. On the basis of a prospective study of 366 patients with endometrial carcinoma, the author postulates that there are two different pathogenetic types of endometrial carcinoma. The first pathogenetic type of the disease arises in women with obesity, hyperlipidemia, and signs of hyperestrogenism: anovulatory uterine bleeding, infertility, late onset of the menopause, and hyperplasia of the stroma of the ovaries and endometrium. The second pathogenetic type of the disease arises in women who have no signs stated above or these signs are not clearly defined. The frequency of the first pathogenetic type in the studied group of women was 65%, whereas the frequency of the second type was 35%. The peculiarities outlined above which are characteristic of the first pathogenetic type of the disease determine the development of highly and moderately differentiated tumors (82.3% G1 and G2), superficial invasion of the myometrium (69.4%), high sensitivity to progestogens (80.2%), and favorable prognosis (85.6% 5-year survival rate). In patients who have the second pathogenetic type of endometrial cancer when endocrine and metabolic disturbances are absent or occult, poorly differentiated tumors arise (62.5% G3), a tendency to deep invasion of tumor into the myometrium is observed (65.7%); high frequency of metastatic spread into the pelvic lymph nodes (27.8%); decrease of sensitivity to progestogens (42.5%); and doubtful prognosis (58.8% 5-year survival rate) are noted.

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Author and article information

Journal

Journal ID (nlm-ta): Cancer Control

Journal ID (hwp): spccx

Journal ID (publisher-id): CCX

Title: Cancer Control : Journal of the Moffitt Cancer Center

Publisher: SAGE Publications (Sage CA: Los Angeles, CA )

ISSN (Print): 1073-2748

ISSN (Electronic): 1526-2359

Publication date (Electronic): 9 May 2022

Publication date Collection: Jan-Dec 2022

Volume: 29

Electronic Location Identifier: 10732748221094797

Affiliations

[1 ]Department of Women’s and Children’s Health, Division of Obstetrics and Gynecology, Karolinska University Hospital, Solna, Ringgold 27106, universityKarolinska Institutet; , Stockholm, Sweden

[2 ]Science for Life Laboratory, Ringgold 27106, universityKarolinska Institutet; , Stockholm, Sweden

[3 ] Ringgold 123495, universityR. E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology of NASU;

[4 ]Department of Microbiology, Tumor and Cell Biology (MTC), Biomedicum, Ringgold 27106, universityKarolinska Institute; , Stockholm, Sweden

[5 ]School of Medical Science, Faculty of Medicine and Health, Ringgold 6233, universityÖrebro University; , Örebro, Sweden

Author notes

[*]Elena Kashuba, Lab of molecular mechanisms of cell transformation, R. E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology of NASU, 45 Vasylkivska str, RE Kavetsky IEPOR of NASU, Kyiv 03022, Ukraine. Email: Elena.Kashuba@ 123456ki.se

[*]Miriam Mints, Women's and Children's Health, Karolinska Institute, Solnavägen 1, Stockholm 17177. Sweden. Email: Miriam.Mints@ 123456ki.se

[*]

These authors contributed equally to the paper

Author information

Igor Govorov https://orcid.org/0000-0003-1809-0270

Elena Kashuba https://orcid.org/0000-0001-7001-4035

Article

Publisher ID: 10.1177_10732748221094797

DOI: 10.1177/10732748221094797

PMC ID: 9092572

PubMed ID: 35533253

SO-VID: 3a63c975-a9fd-48b9-897f-e54363c8f789

License:

This article is distributed under the terms of the Creative Commons Attribution 4.0 License ( https://creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

History

Funding

Funded by: NAS of Ukraine;

Award ID: Research Program 2.2.5.384

Funded by: Cancer Research Foundation (Radiumhemmets Forskningsfonder);

Award ID: 151202

Funded by: Regional Agreement on Medical Training and Clinical Research (ALF);

Award ID: 562083

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typesetter ts10

cover-date January-December 2022

Keywords: endometrial cancer,pkn1,prognostic marker,tumor progression,survival

Data availability:

Keywords: endometrial cancer, pkn1, prognostic marker, tumor progression, survival

Upregulation of PKN1 as a Prognosis Biomarker for Endometrial Cancer

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Abstract

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Cancer Metabolism

Most cited references 23

Cancer statistics, 2019

A pathology atlas of the human cancer transcriptome

Two pathogenetic types of endometrial carcinoma.

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