The androgen-induced protein AIbZIP facilitates proliferation of prostate cancer cells through downregulation of p21 expression

Cui, Xiang; Cui, Min; Asada, Rie; Kanemoto, Soshi; Saito, Atsushi; Matsuhisa, Koji; Kaneko, Masayuki; Imaizumi, Kazunori

doi:10.1038/srep37310

Cited by 20 publications

(26 citation statements)

References 43 publications

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“…32 In addition, Cui et al reported that androgeninduced bZIP, belonging to the CREB/ATF family, facilitated proliferation of prostate cancer cells through downregulation of CDKN1A expression. 34 Our present study demonstrated that the expression of CDKN1A was regulated by CREB in HCC cells. Furthermore, HRH3 downregulated the expression of CDKN1A via inhibiting the phosphorylation of CREB in HCC cells.…”

Section: Discussionsupporting

confidence: 56%

<p>Histamine H3 Receptor Promotes Cell Survival via Regulating PKA/CREB/CDKN1A Signal Pathway in Hepatocellular Carcinoma</p>

2020

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Background: The histamine H3 receptor (HRH3) is mainly expressed in areas of the brain involved in the regulation of the release of various neurotransmitters. Recent studies have shown that HRH3 expression is increased in several types of carcinomas. However, the functional roles and underlying molecular mechanism by which HRH3 regulates cell survival in hepatocellular carcinoma (HCC) remain unknown. Methods: The mRNA and protein expression level of target genes were evaluated by qRT-PCR, Western blot and immunohistochemistry, respectively. Cell viability and cell proliferation activity were assessed by MTS assay and EdU incorporation assay. Cell apoptosis and cell cycle were assessed by flow cytometry analysis. A xenograft mouse model was constructed to investigate the effect of HRH3 on tumor growth in vivo. Results: Our results indicated that HRH3 was significantly upregulated in HCC, which promoted cell survival by accelerating cell proliferation and inhibiting cell apoptosis. Our results also showed that HRH3 in HCC downregulated the expression of cyclin-dependent kinase inhibitor p21 (CDKN1A) to promote G1-S phase transition by inactivating the cAMP/ PKA/CREB pathway, which finally contributed to the malignant growth of HCC. Conclusion: Our findings indicated that HRH3 functioned in promoting HCC survival by inactivating the cAMP/PKA/CREB pathway to downregulate CDKN1A expression. Thus, HRH3 might serve as a potential therapeutic target in HCC treatment.

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Section: Discussionsupporting

confidence: 56%

<p>Histamine H3 Receptor Promotes Cell Survival via Regulating PKA/CREB/CDKN1A Signal Pathway in Hepatocellular Carcinoma</p>

2020

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“…Oestrogen plays an important role in the development and physiology of the normal breast as well as in breast cancer cell proliferation. CREB3L4 has been reported to be highly expressed in sex-related cancers, including prostate, endometrium and uterine cancers [13]. In our experiment, CREB3L4 expression was upregulated in both oestrogen receptorpositive and TNBC cell lines.…”

Section: Discussionsupporting

confidence: 56%

“…As mentioned before, five CREB3 subfamily members have been identified [13]. First, we analysed the differences in the transcription levels of these genes between tumour and normal tissues in multiple types of cancer obtained from the online ONCOMINE database.…”

Section: The Transcription Levels Of Creb3 Subfamily Members In Bcmentioning

confidence: 99%

“…The distinctive CREB3 subfamily consists of five members [11,13]: CREB3 (LZIP/Luman) [14], CREB3L1 (OASIS) [15], CREB3L2 (BBF2H7) [16], CREB3L3 (CREB-H) [17] and CREB3L4 (Tisp40, AIbZIP, or ATCE1) [18]. CREB3L4, a novel human CREB gene, is localized on chromosome 1q21.3 and encodes a protein comprising 395 amino acid residues.…”

Section: Introductionmentioning

confidence: 99%

“…As is typical of other ATF/CREB proteins, CREB3L4 contains a bZIP domain, which is located in its central region (amino acids 222-280). In humans, CREB3L4 is highly expressed in a variety of cancer types, including prostate carcinomas [11,19,20], hepatocellular carcinomas [21] and endometrial cancers [13]. Recently, it was revealed that the high messenger RNA (mRNA) expression of CREB3L4 was associated with reduced relapse-free survival (RFS) and diseasespecific survival (DSS) in BC [22].…”

Section: Introductionmentioning

confidence: 99%

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The Novel Transcription Factor CREB3L4 Contributes to the Progression of Human Breast Carcinoma

Qian

Wang

et al. 2020

J Mammary Gland Biol Neoplasia

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Breast carcinoma(BC)is the most common cancer type among females globally. Understanding the molecular pathways that trigger the development of BC is crucial for both prevention and treatment. As such, the role of transcription factors (TFs) in the development of BC is a focal point in this field. CREB3s play a critical role in initiating the unfolded protein response (UPR); however, the role of CREB3 family members in breast cancer development remains largely unknown. Here, we mined the ONCOMINE database for the transcriptional data of CREB3s in patients with BC. Then, the regulatory functions of a novel TF, CREB3L4, were investigated. CREB3L4 knockdown in MDA-MB-231 and MCF-7 cells suppressed proliferation and promoted apoptosis and cell cycle arrest. ChIP assays confirmed that CREB3L4 can directly bind to the PCNA promoter region, suggesting that the PCNA protein may be functionally downstream of CREB3L4. Additionally, the expression level of CREB3L4 was assessed using our cohort. CREB3L4 is upregulated in breast cancer tissues and is significantly associated with histological grade and tumour size (P = 0.001 and P < 0.001, respectively). Furthermore, PCNA expression was upregulated in breast cancer tissues and positively correlated with CREB3L4. In summary, CREB3L4 may play an important role in the progression of human BC and may serve as a therapeutic target.

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Par14 interacts with the androgen receptor, augmenting both its transcriptional activity and prostate cancer proliferation

et al. 2022

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Background Prostate cancer (PCa) is a major cause of cancer morbidity and mortality for men globally, and androgen signaling clearly drives its onset and progression. Androgen receptor (AR) regulation is complex and remains elusive, despite several studies tackling these issues. Therefore, elucidating the mechanism(s) underlying AR regulation is a potentially promising approach to suppressing PCa. Methods We report that Par14, one isoform of the prolyl isomerases homologous to Pin1, is a critical regulator of AR transcriptional activity and is essential for PCa cell growth. Results Par14 was shown to be overexpressed in PCa, based on analyses of deposited data. Importantly, overexpression of Par14 significantly enhanced androgen‐sensitive LNCap cell growth. In contrast, silencing of Par14 dramatically decreased cell growth in LNCap cells by causing cell cycle arrest. Mechanistically, silencing of the Par14 gene dramatically induced cyclin‐dependent kinase inhibitor p21 at both the mRNA and the protein level through modulating the localization of p53. In addition, suppression of Par14 in LNCap cells was shown to downregulate the expressions of androgen response genes, at both the mRNA and the protein level, induced by dihydrotestosterone. Par14 was shown to directly associate with AR in nuclei via its DNA‐binding domain and augment AR transcriptional activity. Conclusion Thus, Par14 plays a critical role in PCa progression, and its enhancing effects on AR signaling are likely to be involved in the underlying molecular mechanisms. These findings suggest Par14 to be a promising therapeutic target for PCa.

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The androgen-induced protein AIbZIP facilitates proliferation of prostate cancer cells through downregulation of p21 expression

Cited by 20 publications

References 43 publications

<p>Histamine H3 Receptor Promotes Cell Survival via Regulating PKA/CREB/CDKN1A Signal Pathway in Hepatocellular Carcinoma</p>

<p>Histamine H3 Receptor Promotes Cell Survival via Regulating PKA/CREB/CDKN1A Signal Pathway in Hepatocellular Carcinoma</p>

The Novel Transcription Factor CREB3L4 Contributes to the Progression of Human Breast Carcinoma

Par14 interacts with the androgen receptor, augmenting both its transcriptional activity and prostate cancer proliferation

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