Androgen deprivation therapy regulation of β1C integrin expression in prostate cancer

Fuzio, Paolo; Lucarelli, Giuseppe; Perlino, Elda; Battaglia, Michele; Bettocchi, Carlo; Selvaggi, Francesco Paolo; Ditonno, Pasquale

doi:10.3892/or_00000441

Cited by 3 publications

(1 citation statement)

References 21 publications

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“…This activation of integrin β1 promotes tumor metastasis through the involvement of the PI3K/AKT and FAK signaling pathways [77]. In addition, integrin α3β1 also regulates tumor metastasis through the PI3K/AKT/Brn-2 signaling pathway [78]. Breast cancer cells release many extracellular vesicles (EVs), facilitating intercellular communication in the tumor microenvironment and promoting metastasis.…”

Section: Integrin-related Signals In Breast Cancersmentioning

confidence: 99%

Integrins and Actions of Androgen in Breast Cancer

Tsai,

Yang,

Chen

et al. 2023

Cells

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Androgen has been shown to regulate male physiological activities and cancer proliferation. It is used to antagonize estrogen-induced proliferative effects in breast cancer cells. However, evidence indicates that androgen can stimulate cancer cell growth in estrogen receptor (ER)-positive and ER-negative breast cancer cells via different types of receptors and different mechanisms. Androgen-induced cancer growth and metastasis link with different types of integrins. Integrin αvβ3 is predominantly expressed and activated in cancer cells and rapidly dividing endothelial cells. Programmed death-ligand 1 (PD-L1) also plays a vital role in cancer growth. The part of integrins in action with androgen in cancer cells is not fully mechanically understood. To clarify the interactions between androgen and integrin αvβ3, we carried out molecular modeling to explain the potential interactions of androgen with integrin αvβ3. The androgen-regulated mechanisms on PD-L1 and its effects were also addressed.

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Section: Integrin-related Signals In Breast Cancersmentioning

confidence: 99%

Integrins and Actions of Androgen in Breast Cancer

Tsai,

Yang,

Chen

et al. 2023

Cells

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Novel Insights into Autophagy and Prostate Cancer: A Comprehensive Review

Loizzo

Pandolfo

Rogers

et al. 2022

IJMS

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Autophagy is a complex process involved in several cell activities, including tissue growth, differentiation, metabolic modulation, and cancer development. In prostate cancer, autophagy has a pivotal role in the regulation of apoptosis and disease progression. Several molecular pathways are involved, including PI3K/AKT/mTOR. However, depending on the cellular context, autophagy may play either a detrimental or a protective role in prostate cancer. For this purpose, current evidence has investigated how autophagy interacts within these complex interactions. In this article, we discuss novel findings about autophagic machinery in order to better understand the therapeutic response and the chemotherapy resistance of prostate cancer. Autophagic-modulation drugs have been employed in clinical trials to regulate autophagy, aiming to improve the response to chemotherapy or to anti-cancer treatments. Furthermore, the genetic signature of autophagy has been found to have a potential means to stratify prostate cancer aggressiveness. Unfortunately, stronger evidence is needed to better understand this field, and the application of these findings in clinical practice still remains poorly feasible.

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Androgen deprivation therapy affects BCL-2 expression in human prostate cancer

Perlino¹

2011

Int J Oncol

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Abstract. BCL-2 is an integral protein of the external mitochondrial membrane that inhibits cell apoptotic death. We investigated the effect of androgen deprivation therapy (ADT) on BCL-2 expression in prostate cancer tissues. We studied BCL-2 expression in vivo in prostate cancer tissues obtained from patients who underwent radical prostatectomy after neoadjuvant ADT, by Northern and Western blot analysis, and immunohistochemistry. Moreover, gene transcriptional activity was also measured by nuclear run-on experiments. We demonstrated an increase of BCL-2 mRNA expression in patients who underwent neoadjuvant ADT for 1 month in comparison to patients who had not received any therapy. Moreover, we demonstrated that there were no significant modifications of BCL-2 mRNA levels in patients who underwent neoadjuvant ADT for 3 and 6 months. Furthermore, BCL-2 protein levels in patients who underwent neoadjuvant ADT for 1 month were upregulated in comparison to patients who had not received any therapy. Immunohistochemical analysis showed a strong positivity of prostate cells depending on ADT administration for 1 month. Finally, transcriptional activity was not modified in patients who underwent neoadjuvant ADT, suggesting the absence of hormonal regulation on BCL-2 gene expression at the transcriptional level. Our data show that short-term administration of ADT interferes with BCL-2 expression, suggesting that androgen-mediated mechanisms may act through BCL-2-mediated apoptotic pathways. Moreover, since short-term ADT administration does not interfere with BCL-2 expression at the transcriptional level, the androgen-mediated mechanisms involving BCL-2 pathways, probably act at the posttranscriptional level.

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Androgen deprivation therapy regulation of β1C integrin expression in prostate cancer

Cited by 3 publications

References 21 publications

Integrins and Actions of Androgen in Breast Cancer

Integrins and Actions of Androgen in Breast Cancer

Novel Insights into Autophagy and Prostate Cancer: A Comprehensive Review

Androgen deprivation therapy affects BCL-2 expression in human prostate cancer

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