Simple Summary: Lung cancer (LC) represents the leading cause of cancer incidence and mortality worldwide. LC is a lung tumor associated with genetic mutations and environmental (tobacco smoking) or pathological conditions, with poor prognosis and a difficult pharmacological approach. TGF-beta is a molecule that regulates different biological processes at a pulmonary level, and its alteration has been associated with LC development and metastasis. Despite advancements in knowledge of the molecular mechanisms involved in LC, this tumor is still characterized by an unfavorable prognosis and current therapeutic options are unsatisfactory. Some studies have demonstrated that TGF-beta overexpression could be considered a potential predictive marker in LC prognosis, and TGF-beta inhibition has been shown to prevent LC metastasis. Moreover, TGF-beta inhibitors could be used in combination with chemo- and immunotherapy, thereby improving patient survival. Overall, targeting TGF- beta may be a valid possibility to fight LC, and is a novel and effective strategy against this aggressive cancer. Lung cancer (LC) represents the leading cause of cancer incidence and mortality worldwide. LC onset is strongly related to genetic mutations and environmental interactions, such as tobacco smoking, or pathological conditions, such as chronic inflammation. Despite advancement in knowledge of the molecular mechanisms involved in LC, this tumor is still characterized by an unfavorable prognosis, and the current therapeutic options are unsatisfactory. TGF- beta is a cytokine that regulates different biological processes, particularly at the pulmonary level, and its alteration has been demonstrated to be associated with LC progression. Moreover, TGF- beta is involved in promoting invasiveness and metastasis, via epithelial to mesenchymal transition (EMT) induction, where TGF- beta is the major driver. Thus, a TGF- beta-EMT signature may be considered a potential predictive marker in LC prognosis, and TGF- beta-EMT inhibition has been demonstrated to prevent metastasis in various animal models. Concerning a LC therapeutic approach, some TGF- beta and TGF- beta-EMT inhibitors could be used in combination with chemo- and immunotherapy without major side effects, thereby improving cancer therapy. Overall, targeting TGF- beta may be a valid possibility to fight LC, both in improving LC prognosis and cancer therapy, via a novel approach that could open up new effective strategies against this aggressive cancer.

TGF-β as Predictive Marker and Pharmacological Target in Lung Cancer Approach

Ramundo, Valeria
First
;
Palazzo, Maria Luisa;Aldieri, Elisabetta
Last
2023-01-01

Abstract

Simple Summary: Lung cancer (LC) represents the leading cause of cancer incidence and mortality worldwide. LC is a lung tumor associated with genetic mutations and environmental (tobacco smoking) or pathological conditions, with poor prognosis and a difficult pharmacological approach. TGF-beta is a molecule that regulates different biological processes at a pulmonary level, and its alteration has been associated with LC development and metastasis. Despite advancements in knowledge of the molecular mechanisms involved in LC, this tumor is still characterized by an unfavorable prognosis and current therapeutic options are unsatisfactory. Some studies have demonstrated that TGF-beta overexpression could be considered a potential predictive marker in LC prognosis, and TGF-beta inhibition has been shown to prevent LC metastasis. Moreover, TGF-beta inhibitors could be used in combination with chemo- and immunotherapy, thereby improving patient survival. Overall, targeting TGF- beta may be a valid possibility to fight LC, and is a novel and effective strategy against this aggressive cancer. Lung cancer (LC) represents the leading cause of cancer incidence and mortality worldwide. LC onset is strongly related to genetic mutations and environmental interactions, such as tobacco smoking, or pathological conditions, such as chronic inflammation. Despite advancement in knowledge of the molecular mechanisms involved in LC, this tumor is still characterized by an unfavorable prognosis, and the current therapeutic options are unsatisfactory. TGF- beta is a cytokine that regulates different biological processes, particularly at the pulmonary level, and its alteration has been demonstrated to be associated with LC progression. Moreover, TGF- beta is involved in promoting invasiveness and metastasis, via epithelial to mesenchymal transition (EMT) induction, where TGF- beta is the major driver. Thus, a TGF- beta-EMT signature may be considered a potential predictive marker in LC prognosis, and TGF- beta-EMT inhibition has been demonstrated to prevent metastasis in various animal models. Concerning a LC therapeutic approach, some TGF- beta and TGF- beta-EMT inhibitors could be used in combination with chemo- and immunotherapy without major side effects, thereby improving cancer therapy. Overall, targeting TGF- beta may be a valid possibility to fight LC, both in improving LC prognosis and cancer therapy, via a novel approach that could open up new effective strategies against this aggressive cancer.
2023
Inglese
Esperti anonimi
15
8
2295
2309
15
TGF-β; epithelial to mesenchymal transition; lung cancer; marker; metastasis; tumor development
no
1 – prodotto con file in versione Open Access (allegherò il file al passo 6 - Carica)
3
03-CONTRIBUTO IN RIVISTA::03B-Review in Rivista / Rassegna della Lett. in Riv. / Nota Critica
open
262
info:eu-repo/semantics/article
Ramundo, Valeria; Palazzo, Maria Luisa; Aldieri, Elisabetta
File in questo prodotto:
File Dimensione Formato  
cancers-15-02295.pdf

Accesso aperto

Descrizione: Review
Tipo di file: PDF EDITORIALE
Dimensione 2.99 MB
Formato Adobe PDF
2.99 MB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1963930
Citazioni
  • ???jsp.display-item.citation.pmc??? 2
  • Scopus 4
  • ???jsp.display-item.citation.isi??? 4
social impact