Nat Commun: New developments! Inhibiting the TMBIM6 gene inhibits the growth of primary tumors.

Introduction: Tumor markers were discovered in 1978, which refers to tumor-related substances that can be detected in blood, body fluids, and tissues and, at certain levels, reflect the presence of certain tumors.
these tumor markers can also analyze the course of the disease, monitor the efficacy and recurrence, judge the prognosis, to assist in clinical improvement of the patient's further treatment purposes.
recent study published in the journal Nature, the TMBIM6 gene can act as a predictive biomarker for the prognosm of several cancer diseases.
TMBIM6 is an inhibitor of endodernet (ER) stress and was originally named BAX inhibitor (BI)-12.
BI-1/TMBIM6 is a member of the protein-containing 3 family cross-membrane BI-1 sequence.
TMBIM6 is a calcium ion channel-like protein that reduces the stability of calcium ions expressed on the surface of the endoder mesh ER membrane.
it has been raised in many cancer types, including breast, lung, prostate, nasopharyngeal and liver cancers.
previous studies, TMBIM6 overexploitation promoted tumor metastasis by regulating cell mobility and invasiveness, as well as glucose metabolism.
inhibition of TMBIM6 can lead to cell death, thereby reducing tumor occurrence.
, researchers reported transcriptional expressions of Sp1 and PKC-regulated TMBIM68.
PKC is also highly expressed in various cancer types, such as liver, prostate and breast cancer.
although there is much evidence that TMBIM6 is involved in the development of multiple cancers, there is less research on the molecular mechanisms in which TMBIM6 played a role in cancer progress.
target of erythromycin (mTOR) plays a key role in cell metabolism, cell growth and nutritional sensitivity.
mTORC 1 and mTORC2 are two protein complexes with different structures and functions that are often overexposed in cancer and diabetes.
study, the researchers identified TMBIM6 as the primary binding partner of mTORC2 on the ER membrane.
results provide evidence for regulating the activation of AKT and tumor occurring mTORC2-TMBIM6 ICT axis.
to study the carcinogenic effects of TMBIM6 in tumor progression, the researchers first analyzed the TMBIM6 mRNA expression spectrum dataset from multiple tumor samples from NCBI/GEO.
these analyses showed that TMBIM6 was significantly overexposed in fibroblastoma, cervical cancer, endometrial and vultrain cancer, breast, lung and prostate cancer.
, the researchers used tissue microarrays to compare TMBIM6 expression levels in the same tumor tissue and obtained similar results.
TMBIM6 expression in tumor tissue increased the study found that the absence or knock-out of TMBIM6 inhibited the growth of primary tumors.
addition, the activation of mTORC2 is increased by TMBIM6 and stimulates the expression of glycolysis, protein synthesis, lipid synthesis genes, and glycosylated proteins.
In addition, the researchers found that the BIA compound, a potential TMBIM6 antagonist, prevents TMBIM6 from binding to mTORC2, reduces mTORC2 activity, and also regulates the calcium ions leaking from TMBIM6, further inhibiting tumor formation and progression.
TMBIM6 promotes tumor growth.
TMBIM6 activates the AKT path through the mTORC2 cytose axis to evaluate signaling protein molecules that regulate the progress of WT cells and TMBIM6-KO-HT1080 cell tumors.
TMBIM6 regulates the activation of mTORC2 This study shows that TMBIM6 enhances the activity and assembly of mTORC2 by directly binding and stimulating the release of calcium ions.
TMBIM6 limits the growth of primary tumors and damages the metabolism of cancer cells.
, the researchers also found that the small molecular compound BIA is a potential cancer drug that blocks the binding of mTORC2 and TMBIM6.
the study, TMBIM6 regulates sugar metabolism by regulating glycolysis and PPP, which are critical to the activity and signaling of mTORC2.
given the TMBIM6 increase observed in breast, prostate, cervical and lung cancer, metabolic changes mediated by mTORC2, in particular AKT, may be the main mechanism for cancer progression.
addition, the absence of TMBIM6 inhibits the biosynthetics of GSH, which may be more susceptible to reactive oxygen and lipid biosynthetics, thereby inhibiting tumor occurrence.
this study shows that TMBIM6 is an important regulatory factor for regulating mTORC2 activity and the biological energy of tumor cells.
these data show that TMBIM6 has potential clinical value as a predictive biomarker for the prognosm of several cancer diseases.
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