Emodin inhibits the proliferation of papillary thyroid carcinoma by activating AMPK

Abstract

Emodin has been demonstrated to serve antitumor roles in a variety of tumor types, but the effect of emodin on papillary thyroid carcinoma and its molecular mechanisms remain unclear.In the current study, the role of emodin on papillary thyroid carcinoma was analyzed in vitro and in vivo. TPC-1 cells were treated with emodin (0, 10, 25 or 50 µM), and cell viability and apoptosis were detected using Cell Counting Kit-8 and flow cytometry, respectively. The expression levels of AMPK-associated proteins were examined using western blot analysis. To study the effect of emodin on the AMPK pathway, AMPK activator, AICAR and an AMPK inhibitor, Dorsomorphin, were used in TPC-1 cells. In vivo, mice were used to confirm the mechanism of emodin on papillary thyroid carcinoma. The results of the current study indicated that emodin treatment induced cell apoptosis and cell cycle arrest in TPC-1 cells. Furthermore, the inhibitory effect increased in a dose dependent manner. Following emodin treatment, the cell viability of TPC-1 cells was significantly decreased, and apoptosis rate increased (P<0.05). Furthermore, the expression levels of AMPK were increased in the emodin group compared with the control group (P<0.05). Similar effects were observed following AMPK activator treatment in TPC-1 cells. Following AMPK activator treatment, cell proliferation and the cell cycle were inhibited. Also, the AMPK inhibitor was demonstrated to mediate the therapeutic effect of emodin. In addition, the results of the present study demonstrated that emodin inhibited the MEK/ERK pathway. Additionally, the in vivo results of the current study were consistent with those in vitro. In conclusion, the current study demonstrated that the administration of Emodin inhibited the proliferation of papillary thyroid cancer cells via activating AMPK pathway activity.

Topical rhubarb charcoal-crosslinked chitosan/silk fibroin sponge scaffold for the repair of diabetic ulcers improves hepatic lipid deposition in db/db mice via the AMPK signalling pathway

“…By orchestrating processes like the cell cycle, metabolism, and autophagy in cells, AMPK plays a pivotal role in combating both tumors and drug resistance [ 48 – 52 ]. Prior research has confirmed that emodin, a primary active compound found in rhubarb, acts as a regulator of AMPK [ 53 ]. The study demonstrated that emodin, by activating AMPK, led to a decrease in the levels of SREBP1 and FASN proteins in hepatocytes of rats that were given a high-fat diet (HFD).…”

The role of AMPK in cancer metabolism and its impact on the immunomodulation of the tumor microenvironment

“…The metabolic stress induced in cells as a result of increase in the cellular AMP : ATP ratio, due to decreased ATP production, and high levels of intracellular AMP, consequently, leads to the activation of AMPK. The resulting allosteric changes promote the phosphorylation of threonine 172(Thr 172 ) within the activation loop of the AMPK catalytic a-subunit (5). This occurs following the binding of AMP/ ADP to the g-regulatory subunit of AMPK.…”

Traditional Chinese medicine for hypertrophic scars—A review of the therapeutic methods and potential effects

“…As one of the main components of Rheum palmatum L., emodin is widely used in treating inflammatory and non-inflammatory diseases (such as cancer). The potential therapeutic effects of emodin in HS have been elucidated ( Li W. et al, 2021 ; Jiang et al, 2021 ). The researchers used the mouse HS model induced by mechanical stress to study the effect of emodin on HS.…”

“…Its formation and development are closely related to the tissue repair process and involve many regulatory pathways. The formation of a hypertrophic scar (HS) affects the appearance and function of patients’ skin and brings severe physiological and psychological problems to patients ( Li W. et al, 2021 ; Li et al, 2021c ). More than 100 million new cases of scarring occur every year in developing countries ( Zhang et al, 2018 ).…”