TEKT4 Promotes Proliferation, Colony Formation and Metastasis of Papillary Thyroid Carcinoma Cells

TEKT4 seems to promote prostate cancer development, colonisation and translocation. This could mean that TEKT4 is involved in the evolution and dysmorphic characteristics of prostate cancer. TEKT4 can also drive the thyroid gland's metastasis elsewhere by regulating cell migration and tumor growth, which is a key component of the spread and metastasis. TEKT4 can initiate tumor proliferation through changes in cell cycle regulation, or the inhibition of proliferation signals, or by other means, to induce proliferation of cells.

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Tektin 4

TEKT4 (Tektin 4) is a protein from the family of Tektin cells. Tektins are cilia and flagella proteins involved in recombination production and maintenance. TEKT4 can be found in many organisms, but particularly in the ovaries and other tissues. TEKT4 in the cell can build and maintain cell assemblies and also contribute to cell structure and function. TEKT4 might be involved in tumour growth and metastasis in some cancers, particularly pancreatic cancer. Researchers are focusing on the corresponding pathways of action of these cancers.

TEKT4 is a cell recombination protein, which affects cell structure and function. For its function in cancer and, particularly, the spread and proliferation of tumours - scientists are determined to discover its mechanism so that new insights and directions can be taken for treating and studying cancer.

Thyroid Cancer

Thyroid cancer is a cancer that originates in the thyroid tissue and has the potential to metastasize to distant sites. Symptoms include swelling or formation of lumps in the neck. It is important to note that tumors elsewhere may also metastasize to the thyroid gland, but such cancers are not classified as thyroid cancer. The more common primary thyroid cancers can be divided into four categories: papillary thyroid cancer, follicular thyroid cancer, medullary thyroid cancer, and anaplastic thyroid cancer. Less common primary thyroid cancers include Schütler cell carcinoma and thyroid lymphoma.

Physiological Activity of Tektin 4

TEKT4 belongs to the Tektin family, which is involved in cell function and structure. While the exact physiology of TEKT4 is not yet understood, some work has revealed that TEKT4 might participate in key cells' biological functions. These could be physiological functions of TEKT4:

Construction and Maintenance of Cell Buildings

TEKT4 can be engaged in building and repairing cell architecture that regulates cell structure and therefore cell shape, cell movement and intracellular material transportation.

Ciliary and Flagellar Function

We typically think of tektins in terms of cilia and flagella, which are closely related to each other in a lot of different cell types. TEKT4 could be involved in these architectures and functions.

Cell Division and Cell Movement

Because TEKT4 might be part of the recipe for cell division, it could influence the cell division and migration.

Cell Signaling Bursts

We have found Tektins to also be involved in intercellular signalling bursts, and thus TEKT4 could also regulate cell-specific signaling bursts.

Role of Tektin 4 in Papillary Thyroid Cancer

In papillary thyroid cancer (PTC), the role of TEKT4 has not been extensively studied and understood. However, some recent studies suggest that TEKT4 may play a role in certain cancer types, including breast cancer. The expression level of TEKT4 may be associated with the development and progression of some cancers.

Fig. 1 Downregulation of TEKT4 inhibits cell invasion in papillary thyroid cancer cell lines (Zheng, Z., et al.2018).

Thyroid Cancer Cell Migration and Invasion Prevented by Knockdown of Tektin 4

Now the latest findings suggest that knocking down TEKT4 might actually block thyroid tumors' migration and activation. It is these results that TEKT4 could be responsible for thyroid cancer. Here are some possible elicitors:

Stop Cell Migration and Peaking

The migration and peaking capacity of thyroid tumors can be reduced by the inhibition of TEKT4, thus decreasing the expression of thyroid tumors.

Regulating Cell Remodeling and Movement

TEKT4 might regulate critical cell remodeling events by modulating cell structure and motility.

Affecting Tumor Metastasis

Influencing tumor metastasis and dissemination: reducing the expression of TEKT4 could reduce tumor metastasis and dissemination and help patients improve their lymph nodes.

These findings offer both a new function for TEKT4 in thyroid cancer and an opportunity to make the TEKT system a future therapeutic target to prevent thyroid cancer. But it still needs to be confirmed and tested, to see more about the malignant role of TEKT4 in thyroid cancer and whether it might have a clinical function.

Tektin 4 Knockdown Stops the Proliferation and Colonization of TPC1 and BCPAP Cells

The knockdown of TEKT4 suppresses PTC cell proliferation (P 0.05). The cell lines that lack TEKT4 are less proliferative. By TEKT4 knockdown, ischemia and the formation of colonies are blocked in TPC1 and BCPAP. That could imply that TEKT4 contributes to proliferation and colony-building in these cell lines. If you decrease the expression of TEKT4, you might compromise TPC1 and BCPAP's capacity to promote the proliferation of tumors, thus preventing cell growth and proliferation. Dysfunctioning TEKT4 can also alter cell-to-cell contacts and the development of cell colonies, which prevents cells from forming cell colonies. These results will be of help in explaining how TEKT4 operates in thyroid cancer, and suggest an opportunity to use TEKT4 as a target for future treatment to treat thyroid cancer.

Conclusion

Thyroid cancer is the most prevalent endocrine tumour in the world, yet we do not know its molecular mechanism. A number of illnesses are linked to the TEKT4 gene. But it has not been extensively studied in the context of thyroid cancer. This was an attempt to examine TEKT4 in PTC. Proliferation, colony formation, migration and invasion affected the invasion of PTC cell lines TPC1 and BCPAP with small interfering RNA by TEKT4. As our previous research indicates, PTC may depend on TEKT4. TEKT4 deregulation in vitro suppressed cell proliferation, colony-building, cell migration and invasion. We also identified the tumor suppressive effect of TEKT4 knockdown in PTC cell lines with PI3K/Akt inhibition. Our experiments point to TEKT4 being of high biological significance, and worth investigating further.

References

1. Zheng, Z., et al. TEKT4 promotes papillary thyroid cancer cell proliferation, colony formation, and metastasis through activating PI3K/Akt pathway. Endocrine Pathology. 2018, 29: 310-316.
2. Jiang, Y., et al. Enriched variations in TEKT4 and breast cancer resistance to paclitaxel. Nature communications. 2014, 5(1): 3802.