An underlying prognosis predictor of hepatocellular carcinoma: Oncoprotein 18

Gong, Shu; Tao, Zhonghua; Liu, Xiaoyan; Gan, Lin

doi:10.3892/br.2013.197

Cited by 2 publications

(2 citation statements)

References 16 publications

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“…Cell viability were measured as previously described [25,26]. Approximately 4000 stably transfected cells were seeded on 96-well plates.…”

Section: Cell Viability Assaymentioning

confidence: 99%

ADNP prompts the cisplatin-resistance of bladder cancer via TGF-β-mediated epithelial-mesenchymal transition (EMT) pathway

Xie¹,

Zhu²,

Zang³

et al. 2021

J. Cancer

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Activity-dependent neuroprotective protein (ADNP) is vital for embryonic development and brain formation. Besides, the upregulated expression of ADNP enhances tumorigenesis in some human tumors like bladder cancer (BC). However, the potential roles of ADNP in drug resistance and the related mechanisms in BC is unknown. We performed this study to elucidate the influence of ADNP in the chemoresistance of BC and tried to explore the underlying molecular mechanism. The expressions of ADNP in BC from progression and non-progression patient specimens were measured by quantitative real-time PCR (qRT-PCR) and immunohistochemistry (IHC). In vitro experiments including colony formation, cell counting kit-8 (CCK-8), wound healing, and in vivo tumorigenesis assay were performed to explore the effects of ADNP on chemoresistance of BC. The impacts of ADNP on TGF-β/Smad signaling pathways were explored by western blot. Our results showed that the expression of ADNP mRNA and protein were significantly upregulated in BC tissues of the patients who suffered tumor-progression via RT-PCR and western blot. Cox regression survival analysis revealed that patients with high ADNP expression closely linked to shorter tumor-free survival. ADNP downregulation in BC showed more sensitive to cisplatin in vivo, while ADNP overexpression showed the opposite results. Additionally, we confirmed that ADNP promoted cell migration and EMT, thereby inducing cisplatin resistance, which may be related to TGF-β / Smad signaling pathway.

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“…Cell viability were measured as previously described [25,26]. Approximately 4000 stably transfected cells were seeded on 96-well plates.…”

Section: Cell Viability Assaymentioning

confidence: 99%

ADNP prompts the cisplatin-resistance of bladder cancer via TGF-β-mediated epithelial-mesenchymal transition (EMT) pathway

Xie¹,

Zhu²,

Zang³

et al. 2021

J. Cancer

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show abstract

“…MCF-7, MDA-MB-231 and HBL-100 cells were incubated with CCK-8 for the final 3 h before detection. The formazan product was then visualized at the absorbance of 450 nm, and the absorbance was directly proportional to the number of living cells (25,26). Each sample was assayed in triplicate.…”

Section: Reagentsmentioning

confidence: 99%

C5a stimulates the proliferation of breast cancer cells via Akt-dependent RGC-32 gene activation

Lü

2014

Oncology Reports

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Complement system activation contributes to various immune and inflammatory diseases, as well as cancers.However, the role of complement activation in the proliferation of cancer cells is not clear. In the present study, we investigated the consequences of complement activation on the proliferation of breast cancer cells and its possible mechanisms. We focused our study on the potential roles of the anaphylatoxins C3a and C5a in the proliferation of human breast cancer, as two important immune mediators generated after complement activation. Our study revealed that C5a stimulation, but not C3a, enhanced the proliferation of human breast cancer cells in vitro. Moreover, the expression of response gene to complement 32 (RGC-32) was pronounced in breast cancer cells in response to C5a stimulation. Notably, blockade of the C5a receptor markedly reduced the expression of RGC-32 and the proliferation of breast cancer cells stimulated by C5a. Meanwhile, silencing of RGC-32 expression reduced the proliferation of breast cancer cells induced by C5a treatment. Further investigation revealed that Akt activation was involved in C5a-induced RGC-32 expression and breast cancer cell proliferation. In conclusion, the present study indicates that C5a may promote the proliferation of breast cancer cells through Akt1 activation of the RGC-32 gene.

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An underlying prognosis predictor of hepatocellular carcinoma: Oncoprotein 18

Cited by 2 publications

References 16 publications

ADNP prompts the cisplatin-resistance of bladder cancer via TGF-β-mediated epithelial-mesenchymal transition (EMT) pathway

ADNP prompts the cisplatin-resistance of bladder cancer via TGF-β-mediated epithelial-mesenchymal transition (EMT) pathway

C5a stimulates the proliferation of breast cancer cells via Akt-dependent RGC-32 gene activation

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