Editorial, J Clin Immunol Res Vol: 1 Issue: 1

How did I Come Across into Cancer Field?

Leandro Bueno Bergantin^*

Department of Pharmacology, Universidade Federal de São Paulo, Escola Paulista de Medicina, Brazil

*Corresponding Author : Leandro Bueno Bergantin
Department of Pharmacology, Universidade Federal de São Paulo, Escola Paulista de Medicina, Laboratory of Autonomic and Cardiovascular Pharmacology – 55 11 5576-4973
Rua Pedro de Toledo, 669 – Vila Clementino, São Paulo – SP, CEP: 04039-032, Brazil
E-mail: leanbio39@yahoo.com.br

Received: January 27, 2018 Accepted: February 28, 2018 Published: March 05, 2018

Citation: Bergantin LB (2018) How did I Come Across into Cancer Field? J Clin Immunol Res 1:1.

Abstract

Keywords: cancer field, Ca2+/cAMP signalling

At about one decade ago, my starting in research was related to skeletal muscle, including since its physiology until therapeutics for treating muscle wasting conditions. In my MSc studies, I developed a novel experimental model to studying muscle wasting conditions inherited to skeletal muscle, including screening of drugs for alleviating muscle atrophy. In fact, I have studied the role of Ca²⁺/cAMP signalling interaction since then, considering we found that drugs which elevate cAMP levels may alleviate muscle wasting [1]. In my PhD studies, I shifted my studies to smooth muscle, herein studying the role of Ca²⁺/cAMP signalling interaction in its physiology [2]. Herein, we confirmed that elevating cAMP levels may relax smooth muscle, but also enhance the release of transmitter from sympathetic neurons [2]. Here we have coined the term ´calcium paradox´ to explain why in some conditions, as when we use Ca²⁺ channel blockers (CCBs) in low concentrations, these drugs may enhance the contractions of smooth muscle, instead of inhibiting them! We concluded that the Ca²⁺/cAMP signalling interaction properly explain this phenomenon! And the history has gone ahead! Considering CCBs are widely used in clinics as antihypertensive drugs, now we have the possibility to use such drugs for stimulating neurotransmitter release, thus of course these drugs could be used in medical problems related to neurotransmitter release deficit [3-6]. But, now you may ask: ok, but how is this related to cancer field? Now we have gone into the point: Ca²⁺/cAMP signalling interaction has been now well accepted as a fundamental cellular process which exists in virtually many cells, governing the release of neurotransmitter and hormones, muscle contraction, and so on… Yes, there is evidence that such interaction also exists in cancer cells! Most importantly, there is a consensus that Ca²⁺ homeostasis is dysregulated in cancer cells, and strategies which aim to alleviate intracellular Ca²⁺ excess have been considered interesting approaches for inhibiting cancer progression [7,8]. Interestingly, increasing cAMP levels has also been demonstrated to reduce cancer progression [9]. Well, through manipulating Ca²⁺/cAMP signalling interaction, we may alleviate intracellular Ca²⁺ excess, and also increase cAMP levels, a multitarget action, indeed [10-13]! I believe the most interest fact for this approach is the possibility of using CCBs, already approved for other clinical purposes, but now for another medical problem: cancer! In fact, I agree with the phrase: “novel approaches from old pharmaceuticals!”

References

1. Bergantin LB, Figueiredo LB, Godinho RO (2011) The lumbrical muscle: a novel in situ system to evaluate adult skeletal muscle proteolysis and anticatabolic drugs for therapeutic purposes. J Appl Physiol 111: 1710-1718.
2. Bergantin LB, Souza CF, Ferreira RM, Smaili SS, Jurkiewicz NH, et al. (2013) Novel model for "calcium paradox" in sympathetic transmission of smooth muscles: role of cyclic AMP pathway. Cell Calcium 54: 202-212.
3. Bergantin LB, Caricati-Neto A (2016) Challenges for the pharmacological treatment of neurological and psychiatric disorders: Implications of the Ca²⁺/cAMP intracellular signalling interaction. Eur J Pharmacol 788: 255-260.
4. Caricati-Neto A, Garcia AG, Bergantin LB (2015) Pharmacological implications of the Ca²⁺/cAMP signaling interaction: from risk for antihypertensive therapy to potential beneficial for neurological and psychiatric disorders. Pharmacol Res Perspect 3.
5. Bergantin LB (2017) Neurodegenerative diseases: where to go from now? thought provoking through Ca²⁺/camp signaling interaction. Brain Disord Ther 6.
6. Bergantin LB (2017) Neurological disorders: is there a horizon? emerging ideas from the interaction between Ca²⁺ and camp signaling pathways. J Neurol Disord 5.
7. Cui C, Merritt R, Fu L, Pan Z (2017) Targeting calcium signaling in cancer therapy. Acta Pharm Sin B 7: 3-17.
8. Roderick HL, Cook SJ (2008) Ca²⁺ signaling checkpoints in cancer: remodeling Ca²⁺ for cancer cell proliferation and survival. Nat Rev Cancer 8: 361-375.
9. Massimi M, Cardarelli S, Galli F, Giardi MF, Ragusa F, et al. (2016) Increase of intracellular cyclic AMP by PDE4 inhibitors affects hepG2 cell cycle progression and survival. J Cell Biochem 118: 1401-1411.
10. Errante PR, Caricati-Neto A, Bergantin LB (2017) Insights for the inhibition of cancer progression: Revisiting Ca²⁺ and cAMP signalling pathways. Adv Cancer Prevention 2.
11. Errante PR, Francisco S, Caricati-Neto A, Bergantin LB (2017) The pharmacological modulation of Ca²⁺/camp intracellular signaling pathways and traditional antitumoral pharmaceuticals a plausible multi-target combined therapy?. J Clin Exp Oncol 6: 4.
12. Errante PR, Leite AA, Menezes-Rodrigues FS, Caricati-Neto A, Bergantin LB (2017) A novel potential therapeutic target as adjuvant treatment for cancer: the pharmacological interference on the Ca²⁺/cAMP cellular signaling pathways. Enliven: Chall Cancer Detec Ther 2: 1-2.
13. Errante PR, Menezes-Rodrigues FS, Leite AA, Caricati-Neto A, Bergantin LB (2017) The second messengers Ca²⁺ and cAMP as potential therapeutic targets for the control of cancer progression. Adv Cancer Prev 2: 1-2