A significant discovery by researchers at The Medical University of South Carolina (MUSC) Hollings Cancer Center explains why chemotherapy and radiation therapy may not always be effective in curing cancer.
These therapies try to induce cancer cells to commit suicide, but they frequently fall short in the long run because cancer cells are able to adapt, flee, and regrow tumors.
Even though PGCCs have been identified since the development of the microscope and have been seen in malignant tissues, it is unknown how they contribute to the recurrence of cancer.
Recently, a group at Hollings Cancer Center led by Christina Voelkel-Johnson, Ph.D., discovered particular genes that prostate cancer cells alter to become prostate cancer cells that can withstand the stress of therapy.
The group also found that PGCCs can eventually regain their ability to divide cells, which promotes the recurrence of cancer. The Journal of Biological Chemistry published this study.
Recently, researchers at Hollings Cancer Center under the direction of Christina Voelkel-Johnson, Ph.D., found specific genes that prostate cancer cells change to become resistant to the stresses of treatment.
Additionally, the team discovered that PGCCs might gradually restore their capacity for cell division, which encourages the recurrence of cancer. This work was published in the Journal of Biological Chemistry.
Extending the timescale, however, produced the surprising discovery that a huge abnormal-looking cell, previously thought to be “doomed,” really began producing little children over time, even though short-term testing revealed no difference.
These PGCCs could copy their genetic material without dividing their cytoplasm, giving rise to multi-nucleated, larger cells that were morphologically different from typical cancer cells.
Cell-signaling mechanisms that cancer cells use to transform into PGCCs during therapeutic stress and then return to form daughter cells have been discovered by Voelkel-Johnson and her colleagues.
In cancer cells devoid of p53, p21—a crucial protein that p53 typically induces to stop DNA duplication in stressed cells—behaves differently.
Because p21 does not halt damaged DNA duplication in these cells, PGCC production is facilitated. When p21 was blocked, stressed cancer cells were unable to undergo PGCC transformation and produce daughter cells that are in charge of tumor recurrence.
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The research team’s findings point to new therapeutic targets that could enhance patient outcomes after cancer treatment.
Drugs like tamoxifen and statins,
Reference: “Transcriptome analysis of polyploid giant cancer cells and their progeny reveals a functional role for p21 in polyploidization and depolyploidization” by Shai White-Gilbertson, Ping Lu, Ozge Saatci, Ozgur Sahin, Joe R. Delaney, Besim Ogretmen and Christina Voelkel-Johnson, 4 March 2024, Journal of Biological Chemistry. DOI: 10.1016/j.jbc.2024.107136
The study was funded by the National Cancer Institute, the National Institutes of Health, and the American Cancer Society.
which interfere with the described pathways, may be able to prevent recurrence by preventing PGCCs from producing daughter cells, even though directly blocking p21 may not be possible.
According to their research, in order to avoid PGCC formation, these medications should be given in conjunction with radiation therapy or chemotherapy.