Post-thaw viability of in vivo-produced canine blastocysts cryopreserved by slow freezing

Guaitolini, Carlos Renato de Freitas; Taffarel, Marilda Onghero; Teixeira, Natália Soares; Sudano, Mateus José; Freitas, P. Maria Coletto; Lopes, Maria Denise; Landin-Alvarenga, F. da Cruz; Oliveira, Cláudio Alvarenga de; Luz, Marcelo Rezende

doi:10.1016/j.theriogenology.2012.03.003

Cited by 9 publications

(7 citation statements)

References 32 publications

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“…pI/Hoechst33342 double staining was described previously 35 , 36 . Briefly, HCC cells were stained with 5ug/mL pI and 5ug/mL Hoechst33342 after treatment as indicated.…”

Section: Methodsmentioning

confidence: 99%

Chemical and genetic inhibition of STAT3 sensitizes hepatocellular carcinoma cells to sorafenib induced cell death

et al. 2018

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Hepatocellular carcinoma (HCC) has become the second leading cause of cancer related death, with an increasing death rate in recent years. For advanced HCC, sorafenib is the first-line FDA approved drug, with no more than 3 months' overall survival advantage. Recently, a novel strategy has been proposed to improve sorafenib efficacy through enhancing the ability of sorafenib to induce cell death. STAT3 plays a key role in cancer development and recurrence by promoting cell proliferation, survival and immune evasion through its well-established function as a transcription factor in cancer. Notably, STAT3 transcription activity, indicated by its phosphorylation on Y705 is heterogeneous in different liver cancer cell lines. And sorafenib attenuates STAT3 phosphorylation on Y705. However, the role of STAT3 in sorafenib induced cell death is still largely unknown. Here, we show that liver cancer cells also exhibit heterogeneous sensitivities to sorafenib induced cell death, which co-relates with the STAT3-Y705 phosphorylation levels and JAK1/2 expression levels in Hep3B, Huh7 and HepG2 cells. Furthermore, overexpression or knockdown of STAT3 could switch HCC cells between resistant and sensitive to sorafenib induced cell death, which could be partially due to its regulation on Mcl-1, an anti-apoptotic protein. Finally, both inhibitors of STAT3 SH2 domain (S3i-201) or STAT3 upstream kinases JAKs (JAK inhibitor I) could synergistically enhance sorafenib induced cell death. Taken together, these data strongly suggest that STAT3 is not only a downstream effector of sorafenib, but also a key regulator of cellular sensitivity to sorafenib induced cell death, which provide support for the notion to develop STAT3-targeting drugs to improve clinical efficacy of sorafenib in liver cancer.

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“…pI/Hoechst33342 double staining was described previously 35 , 36 . Briefly, HCC cells were stained with 5ug/mL pI and 5ug/mL Hoechst33342 after treatment as indicated.…”

Section: Methodsmentioning

confidence: 99%

Chemical and genetic inhibition of STAT3 sensitizes hepatocellular carcinoma cells to sorafenib induced cell death

et al. 2018

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“…In order to investigate the significance of Pin1 in sorafenib-induced cell death, we stably knocked down Pin1 expression in Huh7, HepG2 and SK-Hep-1 HCC cells using validated Pin1 shRNA lentiviruses, which led to effective Pin1 knockdown, as compared with scrambled shRNA control cells (Figure 2A, 2D and 2G), as described previously [34]. Pin1 knockdown and control cells were treated with 10 μM sorafenib for 72 hours and stained with propidium iodide (pI) and Hoechst33342, which have been previously shown to stain dead/late apoptotic and early apoptotic/normal cells, respectively [35, 36]. Silencing Pin1 expression by genetic knockdown drastically enhanced the ability of sorafenib to induce cell death in these HCC cell lines, as indicated by pI staining (Figure 2B, 2E and 2H).…”

Section: Resultsmentioning

confidence: 61%

“…pI/Hoechst double staining followed by microscopy was performed as previously described [35, 36]. Briefly, HCC cells were treated as indicated and stained with 5 ug/mL pI and 5ug/mL Hoechst 33342, examined under fluorescence microscopy (Zeiss Axio Observer A1).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of the prolyl isomerase Pin1 enhances the ability of sorafenib to induce cell death and inhibit tumor growth in hepatocellular carcinoma

Zheng

Liao

et al. 2017

Oncotarget

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Hepatocellular carcinoma (HCC) is the sixth most common cancer, but is the second leading cause of cancer deaths, partially due to its heterogeneity and drug resistance. Sorafenib is the only medical treatment with a proven efficacy against advanced HCC, but its overall clinical efficacy is still modest. Therefore, a major challenge is how to improve its therapeutic efficacy. The unique prolyl isomerase Pin1 regulates numerous cancer-driving pathways. Notably, Pin1 is overexpressed in about 70% HBV-positive HCC patients and contributes to HCC tumorigenesis. However, the role of Pin1 in the efficacy of sorafenib against HCC is unknown. Here we found that sorafenib down-regulated Pin1 mRNA and protein expression, likely through inhibition of Pin1 transcription by the Rb/E2F pathway. Importantly, Pin1 knockdown potently enhanced the ability of sorafenib to induce cell death in HCC, which was further supported by the findings that Pin1 knockdown led to stabilization of Fbxw7 and destabilization of Mcl-1. Furthermore, all-trans retinoic acid (ATRA), a known anticancer drug that inhibits and ultimately induces degradation of active Pin1 in cancer cells, also potently sensitized HCC cells to sorafenib-induced cell death at least in part through a caspase-dependent manner. Moreover, ATRA also synergistically enhanced the ability of sorafenib to reduce Pin1 and inhibit tumor growth of HCC in mouse xenograft models. Collectively, these results not only demonstrate that Pin1 down-regulation is a key event underlying the anti-tumor effects of sorafenib, but also uncover that Pin1 inhibitors offer a novel approach to enhance the therapeutic efficacy of sorafenib against HCC.

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“…Sampel dari kelompok remaja didominasikan oleh ovarium yang sedang dalam keadaan diestrus atau anestrus dimana oosit dominan berdiameter kecil. Hal ini masuk akal, mengingat diestrus pada anjing biasanya berlangsung selama 2 bulan tanpa kehamilan (Songsasen dan Nagashima, 2020) dan anestrus selama 2-9 bulan sampai siklus berikutnya dimulai (Greer, 2014) dilakukan pewarnaan Giemsa, dan diamati di bawah mikroskop. Jika sel epitel terdiri dari > 90% sel epitel superfisial maka dianggap sedang dalam masa ovulasi (Hu et al, 2020).…”

Section: Morfometri Oosit Anjingunclassified

Morfometri Oosit Anjing pada Berbagai Umur dan Status Kedewasaan Kelamin

Sheren

Susari

Trilaksana

2023

bulvet

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Anjing merupakan salah satu hewan yang sudah ribuan tahun menjadi peliharaan manusia. Tujuan dari penelitian ini untuk mengetahui morfometri oosit anjing dari berbagai umur dan status kedewasaan kelamin. Dalam penelitian ini, 22 pasang sampel ovarium dikoleksi dan disimpan dengan Phosphate Buffer Saline (PBS) sebagai media transport. Oosit dikoleksi menggunakan metode slashing, dimana sayatan-sayatan dibuat pada korteks ovarium dan kemudian dibilas dengan NaCl. Cawan petri berisikan NaCl lalu diamati dibawah mikroskop untuk menemukan oosit. Diameter oosit diambil dengan merata-ratakan dua pengukuran secara tegak lurus satu sama lain. Jika oosit terhalang oleh sel kumulus, pengukuran dilakukan secara diagonal. Pengukuran yang diambil adalah diameter oosit (dengan zona pelusida) dan diameter ooplasma. Berdasarkan analisis statistik pada penelitian ini menggunakan uji one-way ANOVA, menunjukan diameter oosit dan ooplasma dari kelompok prepubertas, <1 tahun pospubertas (remaja), 1-4 tahun (dewasa), dan >4 tahun (tua) hampir tidak bisa dibedakan. Oosit dari anjing dewasa memiliki diameter terbesar (oosit = 108,0±27,8µm dan ooplasma = 85,7±19,5µm) dan secara signifikan lebih besar dibandingkan dengan anjing prepubertas (oosit = 102,5±29,4 µm and ooplasma = 84,8±25,4µm). anjing remaja memiliki diameter terkcil (oosit = 94,1±28,9µm and ooplasma = 78,8±25,3µm), diikuti oleh anjing tua (oosit = 98,5±38,7µm and ooplasma 83,01±35,1µm). Penelitian lanjutan mengenai morfometri oosit diperlukan yang lebih berfokus pada ukuran oosit, siklus estrus, dan kualitas oosit.

show abstract

Post-thaw viability of in vivo-produced canine blastocysts cryopreserved by slow freezing

Cited by 9 publications

References 32 publications

Chemical and genetic inhibition of STAT3 sensitizes hepatocellular carcinoma cells to sorafenib induced cell death

Chemical and genetic inhibition of STAT3 sensitizes hepatocellular carcinoma cells to sorafenib induced cell death

Inhibition of the prolyl isomerase Pin1 enhances the ability of sorafenib to induce cell death and inhibit tumor growth in hepatocellular carcinoma

Morfometri Oosit Anjing pada Berbagai Umur dan Status Kedewasaan Kelamin

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