Overexpression of HepaCAM inhibits cell viability and motility through suppressing nucleus translocation of androgen receptor and ERK signaling in prostate cancer

Song, Xuedong; Wang, Yin; Du, Hongfei; Fan, Yonggang; Yang, Xue; Wang, Xiaorong; Wu, Xiaohou; Luo, Chunli

doi:10.1002/pros.22817

Cited by 22 publications

(24 citation statements)

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“…MAPK is one of the protein kinases which can be stimulated in many kinds of cancer cells and related to tumorigenesis [10][11][12][13]. Smallmolecule inhibitors targeted MAPK have been wildly used for cancer therapeutics as a biologically viable model.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that ERK1/2 acts as nearly 180 different molecules targets and regulates several diverse cellular functions such as cell growth, cell cycle, proliferation, cell death, cell apoptosis, cell adhesion and transcription [9]. In fact, the ERK1/2 plays the above roles in various cancers, such as breast cancer [10], colorectal cancer [11], prostate cancer [12] and lung cancer [13]. However, not all references support the role of activated ERKs in promoting tumorigenesis, and result consistent with the role in tumor suppression has been reported as well [14].…”

Section: Introductionmentioning

confidence: 99%

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ERK1/2 promoted proliferation and inhibited apoptosis of human cervical cancer cells and regulated the expression of c-Fos and c-Jun proteins

et al. 2015

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Small-molecule inhibitors targeted MAPK have been wildly used for some cancer therapeutics as a biologically viable model, but no one has been used for cervical caner. ERK1/2, one of MAPK kinases, is expressed high in cervical cancer tissue. The aim of the present study was to evaluate the effects of ERK1/2 inhibitor U0126 on proliferation and apoptosis of cervical cancer cells and appraise the correlated mechanism of the effects. In this study, the cell proliferation of Hela and C33A cervical cancer cells was tested by Cell Counting Kit-8 (CCK8) assay and cell counting after treated with ERK1/2 inhibitor U0126. The cell cycle and apoptosis were evaluated by flow cytometry (FCM). The protein levels of ERK1/2 and c-Fos and c-Jun were detected by Western blot. The results indicated that after down-regulating ERK1/2 proteins with the inhibitor U0126, Hela and C33A cells proliferation was inhibited, cell apoptosis was promoted, the proportions of G0/G1 stage in cell cycle increased, and G2/M stages decreased. After down-regulating ERK1/2 proteins of Hela and C33A cells, the expression levels of p-c-Fos protein decreased, while p-c-Jun protein increased. The results of this study indicated that ERK1/2 may promote the development of cervical cancer cells, suggesting ERK1/2 inhibitor may be used as an effective target for cervical cancer therapies working for. It might inhibit cervical cancer cells growth via regulating the transcription factors expression of c-Fos and c-Jun.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

ERK1/2 promoted proliferation and inhibited apoptosis of human cervical cancer cells and regulated the expression of c-Fos and c-Jun proteins

et al. 2015

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“…Cell cycle dysregulation is a major factor in cancer cell growth ( 24 ). ERKs have a key role in promoting cell survival and cellular proliferation ( 25 , 26 ) and have been considered to be significant targets for cancer therapeutics ( 27 ). Evidence indicates that erianin affects cell cycle progression, evidenced by inhibition of gastric carcinoma SGC-7901 cell proliferation by blocking progression to S phase ( 28 ), and arresting progression at the G 2 /M phase in hepatocellular carcinoma Huh7 cells ( 23 ) and human colorectal cancer SW480 cells ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Erianin inhibits human cervical cancer cell through regulation of tumor protein p53 via the extracellular signal‑regulated kinase signaling pathway

Peng

et al. 2018

Oncol Lett

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Erianin, a natural bibenzyl compound, is present in Dendrobium chrysotoxum Lindl. (commonly known as Shihu in China), which is used as an antipyretic and analgesic in traditional Chinese medicine, and has been reported to exert inhibitory effects on cancer cells in vitro. Cervical cancer is the third-most common cancer in women worldwide, and has the highest morbidity rate of gynecological malignancies. Thus, the identification of effective chemotherapeutical agents to treat this disease is urgent. The aim of the present study was to elucidate the biological functions and molecular mechanism of erianin on HeLa cells. Cellular proliferation was assessed using an MTT assay and flow cytometry assay with propidium iodide (PI) staining. Apoptosis rates were observed using a high content screening system via annexin V-fluorescein isothiocyanate/PI double staining, and measured by flow cytometry. The protein levels of tumor protein p53, extracellular signal-regulated kinase 1/2 (ERK1/2), caspase-3, B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X (Bax) were assessed by western blot analysis. Erianin inhibited the growth of HeLa cells and induced apoptosis in a dose- and time-dependent manner, inducing cell cycle arrest at the G2/M stage. Erianin treatment also increased the expression of Bax and caspase-3, but decreased levels of Bcl-2 and phosphorylated-ERK1/2. Cells treated with paclitaxel were regarded as the positive group. Together, the results of the present study indicated that erianin could be considered as an effective drug candidate; in HeLa cells it inhibited cellular proliferation and promoted apoptosis via regulation of the ERK1/2 signaling and mitochondrial-based apoptosis pathways. Thus, erianin has the promise to be developed further for cervical cancer therapy.

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“…3d and e ). The former encodes an early growth response TF related among others to lymphocyte development and endothelial cell growth and migration whose downregulation could play a role in the proliferation, metastasis, and progression of cancer cells [ 36 , 37 ], whereas the latter is a likely tumor suppressor gene which codes for a protein involved in cell motility [ 38 ]. Finally, panels F and G illustrate the misregulation of TCF7L1 and DNAJC12 , two significant targets of GATA3 linked to tumorigenesis.…”

Section: Resultsmentioning

confidence: 99%

Circuits of cancer drivers revealed by convergent misregulation of transcription factor targets across tumor types

González-Pérez

2016

Genome Med

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BackgroundLarge tumor genome sequencing projects have now uncovered a few hundred genes involved in the onset of tumorigenesis, or drivers, in some two dozen malignancies. One of the main challenges emerging from this catalog of drivers is how to make sense of their heterogeneity in most cancer types. This is key not only to understand how carcinogenesis appears and develops in these malignancies to be able to early diagnose them, but also to open up the possibility to employ therapeutic strategies targeting a driver protein to counteract the alteration of another connected driver.MethodsHere, I focus on driver transcription factors and their connection to tumorigensis in several tumor types through the alteration of the expression of their targets. First, I explore their involvement in tumorigenesis as mutational drivers in 28 different tumor types. Then, I collect a list of downstream targets of the all driver transcription factors (TFs), and identify which of them exhibit a differential expression upon alterations of driver transcription factors.ResultsI identify the subset of targets of each TF most likely mediating the tumorigenic effect of their driver alterations in each tumor type, and explore their overlap. Furthermore, I am able to identify other driver genes that cause tumorigenesis through the alteration of very similar sets of targets.ConclusionsI thus uncover these circuits of connected drivers which cause tumorigenesis through the perturbation of overlapping cellular pathways in a pan-cancer manner across 15 malignancies. The systematic detection of these circuits may be key to propose novel therapeutic strategies indirectly targeting driver alterations in tumors.Electronic supplementary materialThe online version of this article (doi:10.1186/s13073-015-0260-1) contains supplementary material, which is available to authorized users.

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Overexpression of HepaCAM inhibits cell viability and motility through suppressing nucleus translocation of androgen receptor and ERK signaling in prostate cancer

Cited by 22 publications

References 38 publications

ERK1/2 promoted proliferation and inhibited apoptosis of human cervical cancer cells and regulated the expression of c-Fos and c-Jun proteins

ERK1/2 promoted proliferation and inhibited apoptosis of human cervical cancer cells and regulated the expression of c-Fos and c-Jun proteins

Erianin inhibits human cervical cancer cell through regulation of tumor protein p53 via the extracellular signal‑regulated kinase signaling pathway

Circuits of cancer drivers revealed by convergent misregulation of transcription factor targets across tumor types

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