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Journal : Journal of Stem Cell Research and Tissue Engineering

FUNCTIONAL ROLE OF VIMENTIN'S CYSTEINE IN XIST-MEDIATED EMT INHIBITION IN BREAST CANCER Jayanti; Melisa; Arnando; Mur'ah; Noviyanti
Journal of Stem Cell Research and Tissue Engineering Vol. 9 No. 1 (2025): JOURNAL OF STEM CELL RESEARCH AND TISSUE ENGINEERING
Publisher : Stem Cell Research and Development Center, Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/jscrte.v9i1.73554

Abstract

Breast cancer is the most commonly diagnosed malignancy among women worldwide and a leading cause of cancer-related mortality, primarily due to its high metastatic potential. One mechanism underlying metastasis is the epithelial-to-mesenchymal transition (EMT), which enhances cancer cell mobility, invasiveness, and resistance to treatment. Vimentin, a type III intermediate filament protein, is a hallmark of EMT and plays a structural and regulatory role in cytoskeletal organization and cellular stress responses. Recent studies have highlighted the importance of a single cysteine residue at position 328 (C328) in vimentin, which functions as a redox-sensitive site influencing filament dynamics. However, the role of C328 in cancer progression remained largely unexplored. This literature review investigates the effect of a single amino acid substitution—C328 to serine (C328S)—on breast cancer cell behavior, focusing on findings published between 2020 and 2025, sourced from PubMed and Google Scholar. Evidence from MCF-7 breast cancer cell models reveals that expression of C328S-VIM induces morphological changes, cytoskeletal disorganization, and increased proliferation, migration, and invasion. Notably, C328S-VIM upregulates the long non-coding RNA XIST, which promotes EMT, estrogen independence, and stem-like properties. These findings indicate that the native C328 residue serves a tumor-suppressive function, partly through modulation of XIST activity. Overall, this review presents a novel insight into how a single amino acid mutation in vimentin can reprogram breast cancer cells toward a more aggressive and stem-like phenotype. The study highlights C328 as a potential therapeutic target and broadens our understanding of the molecular mechanisms driving breast cancer progression.
Co-Authors ., Rohaini Adibah, Syifa Adit Widaryono Afiota, Meilita Alex Chandra Alya Azhara Amelia, Lilis Amru Usman Andika Rusli ANDRIANSYAH Anggellya, Febby Anna Cesaria April Lia Hananto Arnando Asriany Atik Rosanti Ayu Anggraini Basriyah, Khusnul Caesare, Muh Raditya Delfa satingi Desi Erawati, Desi Dewiyanti Mitasari Dian Lestari Siregar Dika Setiagraha, Dika Doli Oktamira Dona Sariani Dwi Oktavallyan Eka Safitri, Puput Ersi Sisdianto Fadhilasari, Icha Fanni Tanisya Farid, Muhammad Sultan Felyo, Aldo Fiona Livianti Ghozali, Muhammad Shiddiq Al Gusriyanti, Nabila Hafizah Delyana, Hafizah Hakim, Bustanul Hananto, Agustia Haryadi Sarjono Husain, Hastuti Icha Saswyta Manurung Ika Candra Destiyanti Ikhsan Hidayat Ivan Cristhian Ivori Gracia Simanjuntak Janusi Waliamin Jayanti Khairunnisa, Athalia Shafa Kholifatu Amalia Shofiani, Arisni Leono, Melfinna Lucky Heriyanti Jufri, Lucky Heriyanti Lusi Afriliana M. Faqiul Kamal Maya Marselia Meila Rizqi Adenia Muhammad Aji Al Azhar Muhammad Dicky Syamsuddin Muhammad Haris Saputra Mulia Suryani Mur'ah Nada, Ayu Khusnun Narti Prihartini Ni’matul Fatihah Noferianto Sitompul NOVIYANTI Nur Aisyah, Rohani Nur ‘Azah Nuraini Nuraini Nurfadilah Pakaya Nurhayati Harahap Nurmalia Dewi Nurwijayanti Ony Garindra Saputra Patul, Hali Puspita, Veny Putri Sri Delviani Putri, Aulia Eka Rahmadhani Rangkuti, Saru Noliqo Ratri, Ratri Yulia Ningsih Repina Rey jordi Paputungan Ridwan, Saefatul Riska Yanti Risnita Tri Utami Salsabila Sandy, Chelsea Anggita Nurramah Seri Wahyuni Sintia Safrianti Soeratin, Boyke Setiawan Subriah Tri Yusufi Mardiana Trisna Eka Sari Vidyan Lim Wahyu Alfanda Welan Widya Lestari, Era Wijayadi, Andri Wahyu Yuni Dhea Utari Zulfikar Hasan