Research Paper Volume 16, Issue 8 pp 6773—6795

An LRPPRC-HAPSTR1-PSMD14 interaction regulates tumor progression in ovarian cancer

Dongxiao Li1, , Min Wang1, ,

  • 1 Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China

Received: September 4, 2023       Accepted: February 27, 2024       Published: April 18, 2024
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Copyright: © 2024 Li and Wang. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Ovarian cancer is the second most common cause of gynecologic cancer death. Chemoresistance and metastasis remain major challenges for current treatment. Previously, HAPSTR1 was shown to be a target gene of a paclitaxel resistance-associated miRNA. However, the biological function and underlying molecular mechanisms of HAPSTR1 in ovarian cancer progression remain unclear. Herein, we aimed to measure HAPSTR1 expression in ovarian cancer specimens and examine its correlations with clinical features and key functional interactions with other genes and proteins. An immunohistochemistry assay showed that HAPSTR1 was overexpressed in ovarian cancer tissues and was significantly associated with the FIGO stage and clinical outcome. HAPSTR1 overexpression promoted proliferation, invasion and migration in cellular and mouse models, whereas inhibition induced the opposite effects. In addition, HAPSTR1 stimulated the EMT pathway and affected the expression of autophagy biomarkers. Mechanistically, we demonstrated that HAPSTR1 is bound to LRPPRC and PSMD14 via immunoprecipitation. HAPSTR1 suppressed LRPPRC ubiquitination and recruited PSMD14 to interact with LRPPRC. Moreover, LRPPRC knockdown reversed HAPSTR1-mediated improvement in cellular proliferation, invasion, and migration. Our study is the first detailed and comprehensive analysis of HAPSTR1 in cancer progression and offers an experimental basis for the clinical treatment of ovarian carcinoma.


CCK-8: Cell counting kit-8; COIP: Co-immunoprecipitation; EMT: Epithelial–mesenchymal transition; FIGO: Federation of Gynecology and Obstetrics; GO: Gene Ontology; HAPSTR1: HUWE1-Associated Protein modifying STress Responses; IHC: Immunohistochemistry; KEGG: Kyoto Encyclopedia of Genes and Genomes; LRPPRC: Leucine rich pentatricopeptide repeat containing protein; MS: Mass spectrometry; OV: Ovarian cancer; PTM: Post-translational modification; RT-PCR: Real-time PCR; siRNA: Small interfering RNA; TCGA: The Cancer Genome Atlas.