Identification of proline-rich protein 11 as a major regulator in mouse spermatogonia maintenance via an increase in BMI1 protein stability

Xue, Jiajia; Wu, Tiantian; Huang, Chao; Shu, Minghua; Shen, Cong; Zheng, Bo; Lv, Jinxing

doi:10.1007/s11033-022-07846-8

Cited by 9 publications

(10 citation statements)

References 42 publications

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“…IP assays were carried out according to our previously described procedure [ 16 , 29 ]. Cell lysates were incubated with anti-PTK2 or anti-IgG antibodies overnight, followed by washed beads (Santa Cruz) for 2 h at 4 °C.…”

Section: Methodsmentioning

confidence: 99%

Long non-coding RNA NRSN2-AS1 promotes ovarian cancer progression through targeting PTK2/β-catenin pathway

Wu,

Li,

Liu

et al. 2023

Cell Death Dis

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As a common malignant tumor among women, ovarian cancer poses a serious threat to their health. This study demonstrates that long non-coding RNA NRSN2-AS1 is over-expressed in ovarian cancer tissues using patient sample and tissue microarrays. In addition, NRSN2-AS1 is shown to promote ovarian cancer cell proliferation and metastasis both in vitro and in vivo. Mechanistically, NRSN2-AS1 stabilizes protein tyrosine kinase 2 (PTK2) to activate the β-catenin pathway via repressing MG-53-mediated ubiquitinated degradation of PTK2, thereby facilitating ovarian cancer progression. Rescue experiments verify the function of the NRSN2-AS1/PTK2/β-catenin axis and the effects of MG53 on this axis in ovarian cancer cells. In conclusion, this study demonstrates the key role of the NRSN2-AS1/PTK2/β-catenin axis for the first time and explores its potential clinical applications in ovarian cancer.

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Section: Methodsmentioning

confidence: 99%

Long non-coding RNA NRSN2-AS1 promotes ovarian cancer progression through targeting PTK2/β-catenin pathway

Wu,

Li,

Liu

et al. 2023

Cell Death Dis

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“…After transfection with siRNA, GC-1 and GC-2 cells were seeded in 96-well plates at a density of 4 × 10 3 cells/well. Cell viability was evaluated using a cell counting kit-8 (CCK-8; Beyotime Institute of Biotechnology, Nantong, China), as previously described ( Chen et al, 2022a ; Xue et al, 2022 ; Yu et al, 2022 ). In the colony formation assay, 1,000 transfected cells were placed in 6-well plates; 2 mL DMEM containing 10% FBS was added to each well and changed after 6 d. After 2 weeks, the cells were fixed with methanol and stained with 0.1% crystal violet (Beyotime, Jiangsu, China) for 30 min, and the visible proliferating clumps were counted under a microscope (Carl Zeiss, Oberkochen, Germany).…”

Section: Methodsmentioning

confidence: 99%

Slc26a1 is not essential for spermatogenesis and male fertility in mice

Meng,

Qiao,

Xue

et al. 2023

PeerJ

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Thousands of genes are expressed in the testis of mice. However, the details about their roles during spermatogenesis have not been well-clarified for most genes. The purpose of this study was to examine the effect of Slc26a1 deficiency on mouse spermatogenesis and male fertility. Slc26a1-knockout (KO) mice were generated using CRISPR/Cas9 technology on C57BL/6J background. We found no obvious differences between Slc26a1-KO and Slc26a1-WT mice in fertility tests, testicular weight, sperm concentrations, or morphology. Histological analysis found that Slc26a1-KO mouse testes had normal germ cell types and mature sperm. These findings indicated that Slc26a1 was dispensable for male fertility in mice. Our results may save time and resources by allowing other researchers to focus on genes that are more meaningful for fertility studies. We also found that mRNAs of two Slc26a family members (Slc26a5 and Slc26a11) were expressed on higher mean levels in Slc26a1-KO total mouse testes, compared to Slc26a1-WT mice. This effect was not found in mouse GC-1 and GC-2 germ cell lines with the Slc26a1 gene transiently knocked down. This result may indicate that a gene compensation phenomenon was present in the testes of Slc26a1-KO mice.

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“…The nucleotide sequences of the BAG-targeting siRNAs were as follows: si-BAG3 #1, 5′-AAGAUGCAGUGUCCUUAGG-3′; si-BAG3 #2, 5′-UUGGCUUCUAGCUGUUGGC-3′. The nucleotide sequence of the si-NC was described previously ( Xue et al, 2022 ). Additionally, the pcDNA3.1-BAG3, pcDNA3.1-INTS7, and empty vector (pcDNA3.1-NC) were purchased from GenePharma (Suzhou, China) and used to transfect BMMSCs in Opti-minimum essential medium (MEM; Invitrogen, Carlsbad, CA, USA) using the Lipofectamine 2000.…”

Section: Methodsmentioning

confidence: 99%

“…Migration was assessed using the transwell migration assay, as reported previously ( Wang et al, 2022 ; Xu et al, 2022 ; Xue et al, 2022 ; Zhou et al, 2022b ). Briefly, after transfection for 48 h, 3 × 10 4 cells in 300 µL of serum-free medium were seeded into the upper chamber of each well of a 24-well plate (Merck Millipore), while 700 µL complete medium was added to the lower chamber.…”

Section: Methodsmentioning

confidence: 99%

BAG3 regulates bone marrow mesenchymal stem cell proliferation by targeting INTS7

Liu

et al. 2023

PeerJ

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Background BAG3 is an essential regulator of cell survival and has been investigated in the context of heart disease and cancer. Our previous study used immunoprecipitation-liquid chromatography-tandem mass spectrometry to show that BAG3 might directly interact with INTS7 and regulate bone marrow mesenchymal stem cell (BMMSCs) proliferation. However, whether BAG3 bound INTS7 directly and how it regulated BMMSCs expansion was unclear. Methods BAG3 expression was detected by quantitative real-time PCR in BMMSCs after siRNA-mediated BAG3 knockdown. BMMSC proliferation was determined using the CCK-8 and colony formation assays. The transwell migration, flow cytometry and TUNEL assays were performed to measure BMMSC migration, cell cycle and apoptosis, respectively. Moreover, co-immunoprecipitation, protein half-life assay and western blotting analyses were used to determine the regulatory mechanism underlying the BAG3-mediated increase in BMMSC proliferation. Results The results showed that knocking down BAG3 in BMMSCs markedly decreased their proliferative activity, colony formation and migratory capacity, and induced cell apoptosis as well as cell cycle arrest. Meanwhile, overexpression of BAG3 had the opposite effect. Bioinformatics and BAG3-INTS7 co-immunoprecipitation analyses revealed that BAG3 directly interacted with INTS7. Moreover, the downregulation of BAG3 inhibited the expression of INTS7 and promoted its ubiquitination. We also observed that BAG3 knockdown increased the levels of reactive oxygen species and the extent of DNA damage in BMMSCs. Notably, the upregulation of INTS7 or the addition of an antioxidant scavenger could rescue the BMMSC phenotype induced by BAG3 downregulation. Conclusions BAG3 directly interacts with INTS7 and promotes BMMSC expansion by reducing oxidative stress.

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Identification of proline-rich protein 11 as a major regulator in mouse spermatogonia maintenance via an increase in BMI1 protein stability

Cited by 9 publications

References 42 publications

Long non-coding RNA NRSN2-AS1 promotes ovarian cancer progression through targeting PTK2/β-catenin pathway

Long non-coding RNA NRSN2-AS1 promotes ovarian cancer progression through targeting PTK2/β-catenin pathway

Slc26a1 is not essential for spermatogenesis and male fertility in mice

BAG3 regulates bone marrow mesenchymal stem cell proliferation by targeting INTS7

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