Anti-Müllerian Hormone Signaling Regulates Epithelial Plasticity and Chemoresistance in Lung Cancer

Beck, Tim N.; Korobeynikov, Vladislav A.; Kudinov, Alexander E.; Georgopoulos, Rachel; Solanki, Nehal R.; Andrews-Hoke, Magda; Kistner, Timothy M.; Pépin, David; Donahoe, Patricia K.; Nicolas, Émmanuelle; Einarson, Margret B.; Zhou, Yan; Boumber, Yanis; Proia, David A.; Serebriiskii, Ilya G.; Golemis, Erica A.

doi:10.1016/j.celrep.2016.06.043

Cited by 50 publications

(43 citation statements)

References 65 publications

(93 reference statements)

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“…2d, e). AMH signaling regulates BMP, Akt, NF-κB (nuclear factor-κB), and SMAD signaling in non-smallcell lung cancer cells, and influences cell survival 15 . Csf1 promotes M2-like skewing of macrophage function and inhibits TNF-α expression 16 , and its expression by fibroblasts maintains the stability of macrophage and fibroblast cell populations 17 .…”

Section: Resultsmentioning

confidence: 99%

Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors

et al. 2020

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Idiopathic inflammatory myopathies cause progressive muscle weakness and degeneration. Since high-dose glucocorticoids might not lead to full recovery of muscle function, physical exercise is also an important intervention, but some exercises exacerbate chronic inflammation and muscle fibrosis. It is unknown how physical exercise can have both beneficial and detrimental effects in chronic myopathy. Here we show that senescence of fibro-adipogenic progenitors (FAPs) in response to exercise-induced muscle damage is needed to establish a state of regenerative inflammation that induces muscle regeneration. In chronic inflammatory myopathy model mice, exercise does not promote FAP senescence or resistance against tumor necrosis factor-mediated apoptosis. Pro-senescent intervention combining exercise and pharmacological AMPK activation reverses FAP apoptosis resistance and improves muscle function and regeneration. Our results demonstrate that the absence of FAP senescence after exercise leads to muscle degeneration with FAP accumulation. FAPtargeted pro-senescent interventions with exercise and pharmacological AMPK activation may constitute a therapeutic strategy for chronic inflammatory myopathy.

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Section: Resultsmentioning

confidence: 99%

Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors

et al. 2020

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“…Some reports have suggested a possible role for AMH in cardiovascular prevention in elderly men (Chong et al ., ; Dennis et al ., ), as well as in Klinefelter pre‐pubertal boys (Davis et al ., ) and in premenopausal women (Appt et al ., ): in fact, AMH inversely correlated with the ultrasonographic diameters of the distal‐ and mid‐infrarenal aorta, independently of other markers of Sertoli cell function such as inhibin B (Dennis et al ., ). These results require further confirmation, but are plausible given that AMH has been identified as a potent regulator of TGF‐β/BMP signaling (Beck et al ., ), which is in turn involved in vascular development (Lowery & de Caestecker, ; Cai et al ., ).…”

Section: Beyond Reproduction: Extra Gonadal Pathophysiology Of Amh Anmentioning

confidence: 99%

AMH and INSL3 in testicular and extragonadal pathophysiology: what do we know?

Sansone

Kliesch²,

Isidori

et al. 2019

Andrology

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Background: It is commonly accepted that testicular function is prevalently regulated by the hypothalamic-pituitary-gonadal axis: The pulsatile secretion of GnRH by the hypothalamus induces pituitary expression of the two gonadotropins FSH and LH, which then stimulate Sertoli and Leydig cells, respectively, therefore regulating steroidogenesis and spermatogenesis. However, a growing body of evidence has recently suggested that other hormones act on the reproductive tract since the early phases of fetal development. Anti-M€ ullerian hormone and INSL3 are still largely used only for research purposes despite being increasingly recognized as markers of Sertoli and Leydig cells function, respectively. Objectives: Provide an up-to-date review of the role of anti-M€ ullerian hormone and INSL3 in human pathophysiology according to current evidence. Materials and Methods: A thorough literature review was performed on PubMed, OVID MEDLINE/EMBASE and Google Scholar for papers concerning anti-M€ ullerian hormone and INSL3 in human males. Results: INSL3 is not acutely regulated by the hypothalamic-pituitary axis but is constitutively secreted by Leydig cells, therefore representing a valid marker for their number and status. Anti-M€ ullerian hormone expression, on the other hand, is downregulated by androgens, therefore occurring mostly at the early stages of testicular differentiation and before the onset of puberty. Several conditions affecting testicular development, such as male hypogonadotropic hypogonadism, and their treatment have been associated to specific pattern of INSL3 and anti-M€ ullerian hormone expression, proving a role for both hormones in the diagnostic and therapeutic management. Recent reports suggest a role for both anti-M€ ullerian hormone and INSL3 in extra gonadal physiology, such as cardiovascular and bone health. Conclusion: Anti-M€ ullerian hormone and INSL3 are markers of Sertoli and Leydig cells maturation, respectively, usually involved in the pathogenesis of disorders of sexual differentiation. However, their role in testicular pathology has only been hinted at in the last decades. Recent evidence supports an involvement of both anti-M€ ullerian hormone and INSL3 in extragonadal pathophysiology as well.

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“…обнаружили активность сигнального пути MISRII/АМГ в клетках немелкоклеточного рака лёгкого. Этот каскад оказывает влияние на базальную и BMP-зависимую Smad-сигнализацию и, таким образом, ограничивает эпителиально-мезенхимный переход и участвует в регуляции устойчивости клеток к цитостатикам [82].…”

Section: экспрессия Misrii в норме и при онкопатологияхunclassified

Mullerian inhibiting substance type II receptor as a potential target for antineoplastic therapy

2019

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The review considers properties of the type II anti-Mullerian hormone receptor (mullerian inhibiting substance receptor type II, MISRII), a transmembrane sensor with its own serine/threonine protein kinase activity, triggering apoptosis of the Mullerian ducts in mammalian embryogenesis and providing formation of the male type reproductive system. According to recent data, MISRII overexpression in the postnatal period is found in cells of a number of ovarian, mammary gland, and prostate tumors, and anti-Mullerian hormone (AMH) has a pro-apoptotic effect on MISRII-positive tumor cells. This fact makes MISRII a potential target for targeted anti-cancer therapy. Treatment based on targeting MISRII seems to be a much more effective alternative to the traditional one and will significantly reduce the drug dose. However, the mechanism of MISRII-AMH interaction is still poorly understood, so the development of new anticancer drugs is complicated. The review analyzes MISRII molecular structure and expression levels in various tissues and cell lines, as well as current understanding of the AMH binding mechanisms and data on the possibility of using MISRII as a target for the action of AMH-based antineoplastic drugs.

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Anti-Müllerian Hormone Signaling Regulates Epithelial Plasticity and Chemoresistance in Lung Cancer

Cited by 50 publications

References 65 publications

Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors

Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors

AMH and INSL3 in testicular and extragonadal pathophysiology: what do we know?

Mullerian inhibiting substance type II receptor as a potential target for antineoplastic therapy

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