Abstract
Marsdenia tenacissimae extraction (MTE) as a traditional Chinese herb has long been used to treat some diseases such as tumors in China. However, the potential effectiveness of MTE in leukemia has not yet been fully understood, and the related molecular mechanism is still unknown. In the present study, we aimed to evaluate the effects of MTE on the proliferation and apoptosis of Jurkat cells (T-ALL lines) and lymphocytes from T-ALL (T-cell acute lymphoblastic leukemia) patients. Firstly, CCK8 assays and flow cytometry assays revealed that MTE dose-dependently reduced the proliferation of Jurkat cells by arresting cell cycle at S phase. Secondly, Annexin V-FITC/PI-stained flow cytometry and TUNEL staining assays showed that MTE promoted the apoptosis of Jurkat cells. Mechanistically, MTE enhanced PTEN (phosphatases and tensin homolog) level and inactivated PI3K/AKT/mTOR signaling pathway in Jurkat cells, which mediated the inhibition of cell proliferation by MTE and MTE-induced apoptosis. Finally, MTE significantly inhibited the proliferation and promoted the apoptosis of lymphocytes from T-ALL patients, compared with lymphocytes from healthy peoples. Taken together, these results reveal an unrecognized function of MTE in inhibiting the proliferation and inducing the apoptosis of T-ALL cells, and identify a pathway of PTEN/PI3K/AKT/mTOR for the effects of MTE on leukemia therapy.
Highlights
Acute lymphoblastic leukemia (ALL) is an aggressive tumor of the hematopoietic system
We aimed to evaluate the effects of Marsdenia tenacissimae extraction (MTE) on the proliferation and apoptosis of Jurkat cells (T-ALL lines) and lymphocytes from T-ALL (T-cell acute lymphoblastic leukemia) patients
To examine whether MTE could affect the growth of T-ALL cells, we first performed CCK8 assays by using Jurkat cell lines (T-cell acute lymphoblastic leukemia)
Summary
Acute lymphoblastic leukemia (ALL) is an aggressive tumor of the hematopoietic system. T-cell acute lymphoblastic leukemia (T-ALL) represents a malignant disorder, characterized by an uncontrolled accumulation of T-cell progenitors [1, 2]. Most human cases of T-ALL occur in young children between 2-5 years of age, but T-ALL can occur at any age [3]. The prognosis of pediatric T-ALL has recently improved due to intensified therapies, attaining more than 80% cure rates for children [4], there are many challenges including the early relapse of pediatric T-ALL, the poor prognosis of relapsed and primary chemo-resistant [1]. Less toxic and more efficient and new therapeutic strategies are still required, especially for relapsing and chemo-resistant patients
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