Journals / Uluslararası Hematoloji-Onkoloji Dergisi / 2019 / Cilt: 29 - Sayı: 4

Role of the Rho/Rho-kinase Pathway in Endometrial Adenocarcinoma Cell Proliferation

Endometrial Adenokarsinoma Hücre Proliferasyonunda Rho/Rho-Kinaz Yolağının Rolü

Pages
219–226
Publication Date
2022-11-05
DOI
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Further studies are required to investigate this.

📌 3 Key Takeaways

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Objective & Hypothesis:Present study investigated the possible role of the Rho/ROCK pathway in the proliferation of endometrial adenocarcinoma HEC-1Acells.
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Key Findings & Data:HEC-1A cells were incubated with a ROCK inhibitor, Y-27632(10−7–10−5 M) in the presence and absence of the RhoA activators, lysophosphatidic acid (LPA; 10−6 M) and calpeptin (10−6 M).
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Conclusion & Impact:Further studies are required to investigate this.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Present study investigated the possible role of the Rho/ROCK pathway in the proliferation of endometrial adenocarcinoma HEC-1Acells. Cell proliferation was monitored using the xCELLigence system. HEC-1A cells were incubated with a ROCK inhibitor, Y-27632(10−7–10−5 M) in the presence and absence of the RhoA activators, lysophosphatidic acid (LPA; 10−6 M) and calpeptin (10−6 M). The cellindex was evaluated after incubation for 60, 72, 84, 96, and 108 h. Both LPA and calpeptin significantly increased cell proliferation at60–108 h, which could be reversed by treatment with 10−5 M (but not 10−7 or 10−6 M) Y-27632. On the other hand, Y27632 (10−7–10−5M) alone increased cell proliferation at all the time points tested. Conclusion: The Rho activators, LPA and calpeptin, induced cell proliferation in HEC-1A cells at least in part via ROCK. ROCK inhibitor, Y-27632, reversed the effects of LPA and calpeptin and increasedthe cell index. Further studies are required to investigate this.

Özet

Bu çalışma, Rho/ROCK yolağının endometrial adenokarsinom HEC-1A hücrelerinin proliferasyonundaki olası rolünü araştırmıştır. Hücre proliferasyonu, xCELLigence sistemi kullanılarak izlendi. HEC1A hücreleri, Rho-kinaz (ROCK) inhibitörü, Y-27632 (10–7-10–5 M) ile, RhoA aktivatörleri, lisofosfatidik asit (LPA, 10–6 M) ve calpeptin(10–6 M) varlığında ve yokluğunda inkübe edildi. Hücre indeksi, 60, 72, 84, 96 ve 108 saatlik inkübasyonlarda değerlendirildi. Bulgular: Hem LPA hem de calpeptin, proliferasyonu 60-108 saatler arasında anlamlı şekilde arttırdı. 10–5 M Y-27632 (fakat 10–7 ve 10–6 M değil) LPA ve calpeptinin proliferatif etkisini tersine çevirdi. Öte yandan, Y27632 (10–7-10–5 M) tek başına test edilen tüm zaman noktalarında hücre çoğalmasını arttırdı. Rho aktivatörleri, LPA ve calpeptin, HEC1A hücrelerinde en azından kısmen Rho-kinaz yoluyla hücre proliferasyonunu indüklemiştir. ROCK inhibitörü, Y-27632, LPA ve calpeptinin etkisini tersine çevirdi, ayrıca bu inhibitör, tek başına hücre indeksinde bir artış sağladı. Bu durum daha fazla araştırmayı gerektirmektedir.

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Cite This Article

0000-0001-6442-4185, 0., TIFTIK, R. N., YETKİN, D., BUYUKAFSAR, K. (2022). Role of the Rho/Rho-kinase Pathway in Endometrial Adenocarcinoma Cell Proliferation. Uluslararası Hematoloji-Onkoloji Dergisi, Cilt: 29 - Sayı: 4, 219–226. https://ajindex.com/articles/644766

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References (16)

  1. Braun MM, Overbeek-Wager EA, Grumbo RJ. Diagnosis and Management of Endometrial Cancer. Am Fam Physician 93: 468-474, 2016
  2. DeVita VT, Vincent T, Lawrence et al. Principles & Practice of Oncology, Endometrial Carcinomas, 9th edition. Lippincott Williams & Wilkins, 2011
  3. St-Germain ME, Gagnon V, Mathieu I, et al. Akt regulates COX-2 mRNA and protein expression in mutated-PTEN human endometrial cancer cells. Int J Oncol 24: 1311-1324, 2004
  4. Catalano RD, Wilson MR, Boddy SC, et al. Hypoxia and prostaglandin E receptor 4 signalling pathways synergise to promote endometrial adenocarcinoma cell proliferation and tumour growth. PLoS One 12: 6(5), 2011
  5. Zhou L, Cai B, Bao W, et al. Crosstalk between estrogen receptor and mitogen-activated protein kinase signaling in the development and progression of endometrial cancer. Int J Gynecol Cancer 21: 1357-1365, 2011
  6. Liu Y, Lv L, Xiao W, et al. Leptin activates STAT3 and ERK1/2 pathways and induces endometrial cancer cell proliferation. J Huazhong Univ Sci Technolog Med Sci 31: 365-370, 2011
  7. Yoshizawa Y, Yamada Y, Kanayama S, et al. Signaling pathway involved in cyclooxygenase-2 up-regulation by hepatocyte growth factor in endometrial cancer cells. Oncol Rep 26: 957-964, 2011
  8. Reno EM, Haughian JM, Dimitrova IK, et al. Analysis of protein kinase C delta (PKC delta) expression in endometrial tumors. Hum Pathol 39: 21-29, 2008
  9. Kayaalp O. Kayaalp Rasyonel Tedavi Yönünden Tibbi Farmakoloji. Pelikan Yayincilik. Kanser kemoterapisinin esaslari ve Antineoplastik Ilaçlar 2018. ISBN: 9786055270100
  10. Nicola R, Michael FO. Rho-associated kinases in tumorigenesis: re-considering ROCK inhibition for cancer therapy. EMBO Reports 13: 900-908, 2012
  11. Imamura F, Mukai M, Ayaki M, Akedo H. Y-27632, an inhibitor of Rho-associated protein kinase, suppresses tumor cell invasion via regulation of focal adhesion and focal adhesion kinase. Jpn J Cancer Res 91: 811-816, 2000
  12. Ridley AJ. Rho proteins and cancer. Breast Cancer Res Treat 84: 13-19, 2004
  13. Izawa I, Amano M, Chihara K, Yet al. Possible involvement of the inactivation of the Rho-Rho-kinase pathway in oncogenic Ras-induced transformation. Oncogene 17: 2863-2871, 1998
  14. Fritz G, Just I, Kaina B. Rho GTPases are over-expressed in human tumors. Int J Cancer 81: 682-687, 1999
  15. Burbelo P, Wellstein A, Pestell RG. Altered Rho GTPase signaling pathways in breast cancer cells. Breast Cancer Res Treat 84: 43-48, 2004
  16. Itoh K, Yoshioka K, Ake