Essential role of JunD in cell proliferation is mediated via MYC signaling in prostate cancer cells

Elliott, Bethtrice; Millena, Ana C.; Matyunina, Lilya V.; Zhang, Mengnan; Zhang, Jin; Wang, Guangdi; Zhang, Qiang; Bowen, Nathan J.; Eaton, Vanessa; Webb, Gabrielle; Thompson, Shadyra; McDonald, John F.; Khan, Shafiq A.

doi:10.1016/j.canlet.2019.02.005

Cited by 42 publications

(39 citation statements)

References 91 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been confirmed by studies that NRIP3 and RASL11B play a role in suppressing cancer proliferation in breast cancer and renal cell carcinoma [31,32]. Meanwhile ALPP, JUND, ZBTB7A in gastric cancer, prostate cancer, breast cancer [33][34][35] and other cancers promote the progress of cancer. Thence, we can boldly speculate that PRKACB plays a synergistic role with these tumor suppressors in inhibiting tumor growth.…”

Section: Discussionmentioning

confidence: 90%

Application of cAMP-dependent catalytic subunit β (PRKACB) Low Expression in Predicting Worse Overall Survival: A Potential Therapeutic Target for Colorectal Carcinoma

Yao¹,

Hu²,

Zhang³

et al. 2020

J. Cancer

View full text Add to dashboard Cite

Low expressions of PRKACB are related to the occurrence of various human malignancies. However, the prognostic value of PRKACB expression in colorectal cancer (CRC) patients remains controversial. In this analysis, PRKACB expression in CRC tumors was evaluated across the GEO, TCGA, and Oncomine databases, and a PRKACB survival analysis was performed based on the TCGA profile. We detected PRKACB in 7 GEO series (GSE110225, GSE32323, GSE44076, GSE9348, GSE41328, GSE21510, GSE68468) and TCGA spectra (all P <0.05). A meta-analysis performed in the Oncomine database revealed that PRKACB was significantly up-regulated in neoplastic tissues compared to normal tissues (all P <0.05). A Kaplan-Meier analysis demonstrated that lower PRKACB expression in tumors was significantly associated with poorer overall survival (OS) in patients with CRC (P <0.05). A subgroup analysis showed that low expression of PRKACB correlated with poor 1-, 3-, and 5-year OS (all P <0.05). Furthermore, in males (P = 0.0083), whites (P = 0.0463), and non-mucinous adenocarcinoma patients (P = 0.0108), the down-regulation of PRKACB expression was more significant for the OS prognostic value. Conclusion: PRKACB is down-regulated in tumors and associated with worsening OS in CRC patients.

show abstract

Section: Discussionmentioning

confidence: 90%

Application of cAMP-dependent catalytic subunit β (PRKACB) Low Expression in Predicting Worse Overall Survival: A Potential Therapeutic Target for Colorectal Carcinoma

Yao¹,

Hu²,

Zhang³

et al. 2020

J. Cancer

View full text Add to dashboard Cite

show abstract

“…For example, Elliott B reported that JUND was a crucial modulator in prostate cell cycle progression and thus promoting cancer development. 38 Ishikawa et al found that Butein ameliorated adult leukemia via inhibiting JUND expression. 39 Cheng et al also revealed that JUND was involved in cancer stemness and drug resistance in hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA SNHG7 Functions as an Oncogene in Cervical Cancer by Sponging miR-485-5p to Modulate JUND Expression</p>

Zhao¹,

Zhang²,

Long³

et al. 2020

OTT

View full text Add to dashboard Cite

Background: Long non-coding RNA (LncRNA) SNHG7 is involved in the development of multiple cancers. However, its role in cervical cancer (CC) has not been elucidated. This study aimed to explore the function of SNHG7 in CC progression and the underlying mechanisms. Materials and Methods: The expression levels of SNHG7 and miR-485-5p in CC tissues and cell lines were measured by qPCR. Functional experiments including CCK-8 assay, wound healing assay, transwell assay, flow cytometry, Western blot, luciferases reporter assay and immunoprecipitation (RIP) were performed to explore the SNHG7/miR-485-5p/JUND pathway. Additionally, in vivo study was carried out by establishing tumor xenograft models. Results: We found that SNHG7 was markedly enhanced in CC tissues and cell lines, and associated with poor clinical characteristics. In vitro, knockdown of SNHG7 inhibited CC cell proliferation, migration and invasion, as well as aggravated cell apoptosis. As to mechanism investigation, rescue experiments revealed that miR-485-5p inhibitor could partially reverse the effects on CC cells induced by SNHG7 knockdown. SNHG7 upregulated JUND expression via miR-485-5p. Moreover, tumor xenograft models were established to confirm the findings in vivo. Conclusion: SNHG7 promoted CC progression through miR-485-5p/JUND axis. The SNHG7/miR-485-5p/JUND pathway might provide a novel therapeutic target for CC treatment.

show abstract

“…c-Myc is one of the most important drivers and effectors in promoting the carcinogenesis of pancreatic cancer via the modulation of cell metabolism, cellular growth, metastasis, and apoptosis [46–48] and understanding the regulatory mechanism of c-Myc highlights novel therapeutic strategies for pancreatic cancer. c-Myc is reported to be controlled by many transcriptional factors, including JunD [49], BRD4 [50], and APC [51]. The abnormal activation of oncogenic pathways, such as the PI3K/AKT pathway [52] or MAPK pathway [53], increases c-Myc levels in cancer cells.…”

Section: Discussionmentioning

confidence: 99%

PES1 promotes BET inhibitors resistance and cells proliferation through increasing c-Myc expression in pancreatic cancer

Jin

Fang

Fan

et al. 2019

J Exp Clin Cancer Res

View full text Add to dashboard Cite

sBackgroundOverexpressed PES1 promotes carcinogenesis in various types of malignant tumors. However, the biological role and clinical significance of PES1 in pancreatic cancer are still unexplored.MethodsThe expression level of PES1 in pancreatic cancer cell lines and pancreatic cancer patient samples was determined using Western Blotting analysis, RT-qPCR analysis, immunohistochemical (IHC) analysis of tissue microarray, and the GEPIA web tool. MTS assay, colony formation assay, and xenograft tumor assay were used to evaluate the tumor growth ability of pancreatic cancer cells.ResultsWe established that the expression of PES1 was abnormally increased in pancreatic cancer tissues and led to poor prognosis of pancreatic cancer patients. We also found that PES1 was responsible for promoting cell growth and contributed to bromodomain and cancer cell resistance to extra-terminal (BET) inhibitors in pancreatic cancer. Furthermore, we showed that PES1 interacted with BRD4 to enhance c-Myc expression, which is the primary cause of cancer cell resistance to BET inhibitors in pancreatic cancer. Finally, CDK5 inhibitors were proven to destabilize PES1 and overcome cancer cell resistance to BET inhibitors in pancreatic cancer cells.ConclusionsWe have shown that PES1 could be one of the promoting factors of tumor growth and a prognosis-related protein of pancreatic cancer. Targeting PES1 with CDK5 inhibitors might help overcome cancer cell resistance to BET inhibitors in pancreatic cancer cells.

show abstract

Essential role of JunD in cell proliferation is mediated via MYC signaling in prostate cancer cells

Cited by 42 publications

References 91 publications

Application of cAMP-dependent catalytic subunit β (PRKACB) Low Expression in Predicting Worse Overall Survival: A Potential Therapeutic Target for Colorectal Carcinoma

Application of cAMP-dependent catalytic subunit β (PRKACB) Low Expression in Predicting Worse Overall Survival: A Potential Therapeutic Target for Colorectal Carcinoma

<p>LncRNA SNHG7 Functions as an Oncogene in Cervical Cancer by Sponging miR-485-5p to Modulate JUND Expression</p>

PES1 promotes BET inhibitors resistance and cells proliferation through increasing c-Myc expression in pancreatic cancer

Contact Info

Product

Resources

About