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PC3

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This article is about the cancer cell line PC3. For other uses, see PC3 (disambiguation).
Properties of common prostate cancer cell lines

PC3 or PC-3 is a human prostate cancer cell line used in prostate cancer research and drug development.[1] PC3 cells are useful in investigating biochemical changes in advanced prostate cancer cells and in assessing their response to chemotherapeutic agents. PC3 cells are also used to study viral infection in mammalian cells that exhibit an immune response.[2]


Actin (Phalloidin) and Nuclei (DAPI) staining
PC3 cell cultured in plastic plate

History

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The PC3 cell line was established in 1979 from lumbar vertebral metastasis of grade IV prostatic adenocarcinoma in a 62-year-old Caucasian male.[3][4]

Responses and behaviours

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These cells do not respond to androgens, glucocorticoids or fibroblast growth factors,[5] but results suggest that the cells are influenced by epidermal growth factors.[6] PC3 cells have high metastatic potential [7] [a] Comparisons of the protein expression of PC3, LNCaP, and other cells have shown that PC3 is characteristic of small cell neuroendocrine carcinoma.[5]

PC3 cells have low testosterone-5-alpha reductase and acidic phosphatase activity, and do not express PSA (prostate-specific antigen).

Characteristics

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Karyotypic analysis: near-triploid, having 62 chromosomes. [b] Expression of CK7, CK8, CK18, and CK19, non AR and PSA. From a morphological point of view, electron microscopy revealed that PC3 cells show characteristics of a poorly-differentiated adenocarcinoma. Tumor size approximately 100 % increase: approximately 33 h. [4] They have features common to neoplastic cells of epithelial origins, such as numerous microvilli, junctional complexes, abnormal nuclei and nucleoli, abnormal mitochondria, annulate lamellae, and lipoidal bodies.[citation needed] Q-band analysis showed no Y chromosome.

Lines of PC3 cells

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There are a variety of Different PC3 cell lines derived from the original PC3 cell line. The most common include PC3-PR Cells, PC-3M Cells, PC3-EGFP Cells, PC3-Dox Cells, PC3-LacZ Cells, PC3-AR Cells. Each of these have different morphological and physiological properties but they all originate from the original PC3 cell derived from the 62-year old caucasian male.[3]

PC3-PR Cells (Paclitaxel-Resistant)

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C3-PR cells are Paclitaxel-Resistant cells that, unlike PC3 cells, are resistant with Paclitaxel (PTX). In these cells PTX is unable to stimulate p21 and acetylated α-tubulin expression of PC3-PR cells. Though Cabazitaxel and HDAC inhibitors were able to induce p21 and α-tubulin, these equally suppress PC3-PR cells. Due to the suppression ability of Cabazitaxel and HDAC, these drugs are able to replace the common chemotherapy drug in PC3-PR cells.[8] These cells allow researchers to develop strategies in order to treat prostate cancer that is resistant to traditional chemotherapy drugs.

PC-3M Cells (Metastatic)

PC-3-M cells are a highly metastatic form of PC3 cells. They metastasize in a much more prolific fashion than regular PC3 cells. These cells are used in research to study the potential treatments of PC's that are highly metastatic. PC3-M is used in research from in-vitro to in-vivo model animals for cancer research.[9] This cell line is able to research the most dangerous, advanced forms of pancreatic cancer, as the high metastasis potential will allow these cells to spread throughout the body in a rapid fashion.

PC3-EGFP Cells (Enhanced Green Fluorescent Protein)

PC3-EGFP are PC3 cells that have been modified in order to express green fluorescent proteins at a higher rate. This is visible when EGFP expression levels are analyzed.[10] This allows for live tracking of PC3 cells as well as real time imaging. This can be especially useful when studying the proliferation as well as the drug response in PC3 cells.

PC3-Dox Cells

PC3-Dox cells are modified to be resistant to Doxorubicin. This cell line is used to study multidrug resistance (MDR) in PC3. Specifically miR-21 research is based on this lineage of cells in order to determine if it is possible to reverse (MDR) through the employment of this drug. Additionally these cells look at if it is possible to resensitize PC3 cells to Doxorubicin.[11]

PC3-Ras Cells PC3-Ras cells are modified in order to express the oncogene ras. Ras is involved in the activation of downstream effectors that play a role in DNA transcription. This modification allows researchers to study the role of Ras signaling in prostate cancer. This is very important to studying the processes of tumor progression, metastasis, and drug resistance in pancreatic cancer cells, as it is tied to mitosis.[12]

Applications in science

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PC3 cells can be used to create subcutaneous tumor xenografts in mice to investigate the tumor environment and therapeutic drug functionality.[13]

Significance of PC3 in Prostate Cancer Research

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Prostate cancer (PC) is the most common form of non-cutaneous malignant cancer in males, and is the second leading cause of cancer deaths in males.[14] PC3 cells have been utilized to research aggressive and castration-resistant forms of prostate cancer. The androgen-independence of these cells during cell division makes them invaluable for studying the molecular mechanisms embedded in studying advanced prostate cancer.[15] PC3 cells have been involved in research regarding the prevention and treatment of prostate cancer. PC3 cells have been used in research surrounding Methylene Blue Photodynamic Laser Therapy (MB-PDT) and Sulforaphane (SFN). Research published in 2023 utilizing PC3 cells illustrated that MB-PDT treatment decreased the antioxidant potential and increased lipid peroxidation, decreasing the viability and metastatic capacity of PC3 cells. The results from this study further support other research that MB-PDT can be used in conjunction with traditional therapies to treat aggressive versions of prostate cancers.[16] SFN treatments have been used to treat prostate cancer as well as many other tumors. SFN is a plant-derived chemical present in many plants, especially broccoli and broccoli sprouts; though there are concerns about the bioavailability of SFN supplements.[17] Nevertheless, many prostate cancer patients have turned to SFN to prevent growth of PCs resistant to many of the traditional forms of treatment. Experimentation in 2020 linked SFN to a decrease in prostate cancer proliferation and growth, using PC3 cells alongside DU145. These studies found that using treatments as low as 1 μM of SFN decreased PC3 cell count by 50% in-vitro.[18]

in vitro study

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Treatment by quercetin induced various tumor suppressor genes including transforming growth factor β receptor 11, [19] and quenched reactive oxygen species. [20]

See also

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Notes

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  1. ^ DU145 cells have a moderate potential, LNCaP, low.[7]
  2. ^ Donkeys, Lymantria dispar, Scarlet macaws all naturally have 62 chromosomes (see: List of organisms by chromosome count)

References

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  1. ^ Korsnes, Mónica Suárez; Ramberg, Håkon André; Taskén, Kristin Austlid; Korsnes, Reinert (2024-12-02). "Video tracking of single cells to identify clustering behavior". Frontiers in Imaging. 3 1443142. doi:10.3389/fimag.2024.1443142. hdl:10852/114893. ISSN 2813-3315.
  2. ^ Timm C, Gupta A, Yin J (August 2015). "Robust kinetics of an RNA virus: Transcription rates are set by genome levels". Biotechnology and Bioengineering. 112 (8): 1655–62. Bibcode:2015BiotB.112.1655T. doi:10.1002/bit.25578. PMC 5653219. PMID 25726926.
  3. ^ a b Kaighn ME, Narayan KS, Ohnuki Y, Lechner JF, Jones LW (July 1979). "Establishment and characterization of a human prostatic carcinoma cell line (PC-3)". Investigative Urology. 17 (1): 16–23. PMID 447482.
  4. ^ a b Alakesh Bera; et al. (17 September 2020). "Cellular and Molecular Progression of Prostate Cancer: Models for Basic and Preclinical Research". Cancers (Basel). 12 (9). MDPI: 2651. doi:10.3390/cancers12092651. PMID 32957478. 3. Prostate Cancer Research Models Androgen-Receptor Non-Expressing developed from lumbar vertebral metastasis of a grade IV prostatic adenocarcinoma from a 62-year-old Caucasian man [100].In the karyotypic analysis, these cells were found to be near triploid having 62 chromosomes. PC3 cells express CK7, CK8, CK18, and CK19 but not AR and PSA and exhibit characteristics of a poorly differentiated adenocarcinoma with a doubling time of about 33 h [138,139].
  5. ^ a b Tai S, Sun Y, Squires JM, Zhang H, Oh WK, Liang CZ, Huang J (November 2011). "PC3 is a cell line characteristic of prostatic small cell carcinoma". The Prostate. 71 (15): 1668–79. doi:10.1002/pros.21383. PMC 3426349. PMID 21432867.
  6. ^ Johnston ST, Shah ET, Chopin LK, Sean McElwain DL, Simpson MJ (July 2015). "Estimating cell diffusivity and cell proliferation rate by interpreting IncuCyte ZOOM assay data using the Fisher-Kolmogorov model". BMC Systems Biology. 9 (38): 38. doi:10.1186/s12918-015-0182-y. PMC 4506581. PMID 26188761.
  7. ^ a b Clayton W. Molter; Allen J. Ehrlicher (February 12, 2021). "The Mechanics of Prostate Cancer Progression: Toward Characterizing Metastatic Potential as a Function of Cell Contractility". Biophysical Journal. 12 (3, Supplement 1). Elsevier: 168a. Bibcode:2021BpJ...120R.168M. doi:10.1016/j.bpj.2020.11.1192.
  8. ^ Sobue, Sayaka; Mizutani, Naoki; Aoyama, Yuka; Kawamoto, Yoshiyuki; Suzuki, Motoshi; Nozawa, Yoshinori; Ichihara, Masatoshi; Murate, Takashi (October 2016). "Mechanism of paclitaxel resistance in a human prostate cancer cell line, PC3-PR, and its sensitization by cabazitaxel". Biochemical and Biophysical Research Communications. 479 (4): 808–813. Bibcode:2016BBRC..479..808S. doi:10.1016/j.bbrc.2016.09.128. ISSN 0006-291X. PMID 27687545.
  9. ^ Chu, Jian Hong; Sun, Zu Yue; Meng, Xue Lian; Wu, Jian Hui; He, Gui Lin; Liu, Gui Ming; Jiang, Xiu Rong (February 2006). "Differential metastasis-associated gene analysis of prostate carcinoma cells derived from primary tumor and spontaneous lymphatic metastasis in nude mice with orthotopic implantation of PC-3M cells". Cancer Letters. 233 (1): 79–88. doi:10.1016/j.canlet.2005.03.034. ISSN 0304-3835. PMID 15885894.
  10. ^ Karimov, Michael; Scherer, Marlene; Franke, Heike; Ewe, Alexander; Aigner, Achim (2023). "Analysis of polymeric nanoparticle properties for siRNA/DNA delivery in a tumor xenograft tissue slice air–liquid interface model". Biotechnology Journal. 18 (4) 2200415. doi:10.1002/biot.202200415. ISSN 1860-7314. PMID 36541426.
  11. ^ Zhao, Weichong; Ning, Lei; Wang, Lihui; Ouyang, Tao; Qi, Lei; Yang, Ruihong; Wu, Yanlin (June 2021). "miR-21 inhibition reverses doxorubicin-resistance and inhibits PC3 human prostate cancer cells proliferation". Andrologia. 53 (5) e14016. doi:10.1111/and.14016. ISSN 1439-0272. PMID 33598946.
  12. ^ Pamonsinlapatham, Perayot; Gril, Brunilde; Dufour, Sylvie; Hadj-Slimane, Réda; Gigoux, Véronique; Pethe, Stéphanie; L'Hoste, Sébastien; Camonis, Jacques; Garbay, Christiane; Raynaud, Françoise; Vidal, Michel (2008-11-01). "Capns1, a new binding partner of RasGAP-SH3 domain in K-RasV12 oncogenic cells: Modulation of cell survival and migration". Cellular Signalling. 20 (11): 2119–2126. doi:10.1016/j.cellsig.2008.08.005. ISSN 0898-6568. PMID 18761085.
  13. ^ Germain, Lucas; Lafront, Camille; Paquette, Virginie; Neveu, Bertrand; Paquette, Jean-Sébastien; Pouliot, Frédéric; Audet-Walsh, Étienne (August 2023). "Preclinical models of prostate cancer — modelling androgen dependency and castration resistance in vitro, ex vivo and in vivo". Nature Reviews Urology. 20 (8): 480–493. doi:10.1038/s41585-023-00726-1. ISSN 1759-4820. PMID 36788359.
  14. ^ Cooperberg, Matthew R.; Park, Sangtae; Carroll, Peter R. (September 2004). "Prostate cancer 2004: insights from national disease registries". Oncology. 18 (10). Williston Park, N.Y.: 1239–1247, discussion 1248–1250, 1256–1258. ISSN 0890-9091. PMID 15526829.
  15. ^ Tai, Sheng; Sun, Yin; Squires, Jill M.; Zhang, Hong; Oh, William K.; Liang, Chao-Zhao; Huang, Jiaoti (2011). "PC3 is a cell line characteristic of prostatic small cell carcinoma". The Prostate. 71 (15): 1668–1679. doi:10.1002/pros.21383. ISSN 1097-0045. PMC 3426349. PMID 21432867.
  16. ^ de Melo Gomes, Laura Calazans; de Oliveira Cunha, Amanda Branquinho; Peixoto, Luiz Felipe Fernandes; Zanon, Renata Graciele; Botelho, Françoise Vasconcelos; Silva, Marcelo José Barbosa; Pinto-Fochi, Maria Etelvina; Góes, Rejane Maira; de Paoli, Flávia; Ribeiro, Daniele Lisboa (June 2023). "Photodynamic therapy reduces cell viability, migration and triggers necroptosis in prostate tumor cells". Photochemical & Photobiological Sciences. 22 (6): 1341–1356. Bibcode:2023PhPhS..22.1341D. doi:10.1007/s43630-023-00382-9. ISSN 1474-9092. PMC 9983546. PMID 36867369.
  17. ^ Clarke, John D.; Hsu, Anna; Riedl, Ken; Bella, Deborah; Schwartz, Steven J.; Stevens, Jan F.; Ho, Emily (November 2011). "Bioavailability and inter-conversion of sulforaphane and erucin in human subjects consuming broccoli sprouts or broccoli supplement in a cross-over study design". Pharmacological Research. 64 (5): 456–463. doi:10.1016/j.phrs.2011.07.005. ISSN 1096-1186. PMC 3183106. PMID 21816223.
  18. ^ Rutz, Jochen; Thaler, Sarah; Maxeiner, Sebastian; Chun, Felix K.-H.; Blaheta, Roman A. (2020-11-18). "Sulforaphane Reduces Prostate Cancer Cell Growth and Proliferation In Vitro by Modulating the Cdk-Cyclin Axis and Expression of the CD44 Variants 4, 5, and 7". International Journal of Molecular Sciences. 21 (22): 8724. doi:10.3390/ijms21228724. ISSN 1422-0067. PMC 7699211. PMID 33218199.
  19. ^ Hari Krishnan Nair; et al. (Jan 2004). "Inhibition of Prostate Cancer Cell Colony Formation by the Flavonoid Quercetin Correlates with Modulation of Specific Regulatory Genes". Clin Diagn Lab Immunol. 11 (1). American Society for Microbiology: 63–69. doi:10.1128/CDLI.11.1.63-69.2004. PMID 14715546.
  20. ^ Simona Izzo; Valeria Naponelli; Saverio Bettuzzi (2020). "Flavonoids as Epigenetic Modulators for Prostate Cancer Prevention - 2.2.1. Anti-Oxidant and Pro-Oxidant Activity". Nutrients. 12 (4). MDPI. doi:10.3390/nu12041010. PMC 7231128. PMID 32268584.
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